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Cardiac-disease-induced posttraumatic stress symptoms (CDI-PTSS) have been detected among a substantial number of cardiac patients. Even though patients' caregiving partners are also susceptible to CDI-PTSS, the research on cardiac partners' CDI-PTSS is scarce. Based on the ecological model of trauma and recovery, we investigated levels of partners' CDI-PTSS over time, and factors that potentially contribute to it.During patients' hospitalizations, partners (A mild level of CDI-PTSS was detected among partners, 4 and 8 months after patients' cardiac event. Partners' distress as measured during patients' hospitalization, and their fear of patients' illness progression, contributed to the manifestation of CDI-PTSS over time.The findings shed light on potential risk factors for partners' CDI-PTSS. Interventions to ameliorate partners' distress and fear of illness progression should be designed toward reducing the development of CDI-PTSS among partners. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Objectives: The fact that spousal support is not always beneficial for the recipient continues to intrigue researchers in the dyadic support field. One possible explanation for this phenomenon may be individual differences in attachment orientations, which might promote or, conversely, hinder the ability to capitalize on one’s partner’s support. We therefore assessed the interactive contribution of cardiac patients’ attachment orientations (anxious and avoidant) and partners’ caregiving styles (sensitive and compulsive) to patients’ anxiety symptoms 6 months after a first acute coronary syndrome (ACS). Design and methods: A longitudinal design was employed among 114 couples coping with one partner’s ACS. During hospitalization, patients completed the Experiences in Close Relationships scale, tapping attachment orientation, and 6 months later, the anxiety scale of the Brief Symptom Inventory. Partners completed the Adult Caregiving Questionnaire during patients’ hospitalization. Results: Regression analyses showed that partners’ caregiving styles moderated the positive association between patients’ anxious attachment and anxiety symptoms. This association was stronger when partners were characterized with high levels of compulsive caregiving, but also, and surprisingly, when partners were characterized with high levels of sensitive caregiving. No significant effects were found for highly avoidant patients. Conclusions: The findings suggest that patients’ personalities play a crucial role in determining the consequences of partners’ caregiving styles. Integrating the personality perspective into the dyadic paradigm may allow a more comprehensive understanding of the circumstances under which partners’ care reduces patients’ distress.

Objective Cardiac disease induced post-traumatic stress symptoms (CDI-PTSS) have been associated with negative consequences for patients’ mental and physical health. Identifying risk factors as well as potential buffers is necessary for understanding the development and maintenance of CDI-PTSS. The current study focused on the mediating and moderating role played by patients’ perceptions of their partners’ ways of providing support (active engagement, overprotection, and protective buffering) in the development and stabilization of CDI-PTSS levels over time. Method Male patients ( N = 106) were recruited at hospitalization (T1) and completed the study’s questionnaires at two time points: approximately four months after hospital discharge (T2) and approximately eight months after discharge (T3). Results Structual equation modeling was used to test the study hypotheses. All three forms of T2 perceived partner support were positively associated with T2 CDI-PTSS levels which, in turn, were positively associated with T3 CDI-PTSS levels. The linear association between T2 and T3 CDI-PTSS was positive but decreased as perceived partner protective buffering levels increased. Conclusions In the context of CDI-PTSS, perceived partner support seems to have a different effect than it has in non-traumatic illness contexts. Interventions for couples coping with CDI-PTSS should be designed accordingly.

Background The additional prognostic value of resting electrocardiogram (ECG) in long-term cardiovascular disease (CVD)-risk-assessment is unclear. We evaluated the association of incidental abnormal ECG findings with long-term CVD-risk and all-cause mortality, and assessed the additional prognostic value of ECG as a screening tool in adults without known CVD. Methods A cohort of 2601 Israeli men and women without known CVD were actively followed from 1976 to 1982 for 23-year cumulative CVD-incidence, and until May 2017 for all-cause mortality. At baseline and follow-up, participants underwent interviews, physical examinations, blood tests and ECG. Results At baseline, 1199 (46.1%) had incidental abnormal ECG findings (exposed-group). CVD cumulative incidence reached 31.6% among the 930 survivors who participated in the active follow-up (294/930). During a 31-year median follow-up, 1719 (66.1%) of the total cohort died. Incidental abnormal ECG findings were associated with 46% greater CVD-risk (odds ratio = 1.46, 95%CI = 1.09–1.97). The net reclassification improvement (NRI) of CVD-risk was 7.4% (95%CINRI = 1.5%–13.3%, p = 0.01) following the addition of ECG findings, but the C-index improvement was not statistically significant [C-index = 0.656 (0.619–0.694) vs. C-index = 0.666 (0.629–0.703), p = 0.14]. Multivariable Cox regression demonstrated an all-cause mortality hazard ratio (HR) of 1.18 (95%CI = 1.07–1.30) for exposed vs. unexposed individuals. Non-specific T-wave changes and left-axis deviation are the incidental ECG abnormalities that were associated with all-cause mortality [HR = 1.18 (95%CI = 1.05–1.33) and HR = 1.19 (95%CI = 1.00–1.42), respectively]. Conclusion Incidental abnormal ECG findings, mainly non-specific T-wave changes and left-axis deviation, were associated with increased long-term CVD-risk and all-cause mortality among individuals without known CVD, and demonstrated net reclassification improvement for CVD-risk.

Aim There is a clinical need for safety data regarding hydroxychloroquine (HCQ) and chloroquine (CQ) during the coronavirus (COVID-19) pandemic. We analysed real-world data using the U.S. Food and Drug Administration Adverse Events Reporting System (FAERS) database to assess HCQ/CQ-associated cardiovascular adverse events (CVAEs) in pre-COVID-19 reports. Methods We conducted disproportionality analysis of HCQ/CQ in the FAERS database (07/2014-9/2019), using reporting odds ratio (ROR) and the lower bound of the information component 95% credibility interval (IC025 ). Results The full database contained 6 677 225 reports with a mean (±SD) age of 53 (±17) years and 74% females. We identified 4895 reports of HCQ/CQ related adverse events, of which 696 (14.2%) were CVAEs. Compared with the full database, HCQ/CQ use was associated with a higher reporting rate of major CVAEs, including cardiomyopathy (n = 86 [1.8%], ROR = 29.0 [23.3-35.9]), QT prolongation (n = 43 [0.9%], ROR = 4.5 [3.3-6.1]), cardiac arrhythmias (n = 117 [2.4%], ROR = 2.2 [1.8-2.7]) and heart failure (n = 136 [2.8%], ROR = 2.2 [1.9-2.7], all IC₀₂₅ > 0). No statistically significant differences were observed between sex and age groups. CVAEs were reported more often in patients with systemic lupus erythematosus and Sjogren's syndrome. HCQ/CQ-associated CVAEs demonstrated subsequent hospitalization and mortality rates of 39% and 8%, respectively. Overdose reports demonstrated an increased frequency of QT prolongation and ventricular arrhythmias (35% and 25%, respectively). Conclusion In a real-world setting, HCQ/CQ treatment is associated with higher reporting rates of various CVAEs, particularly cardiomyopathy, QT prolongation, cardiac arrhythmias and heart failure. HCQ/CQ-associated CVAEs result in high rates of severe outcomes and should be carefully considered as an off-label indication, especially for patients with cardiac disorders.

Background: The experience of an acute coronary event (ACE), including early care and evaluation, can be a distressing and traumatic experience for patients and their romantic partners, who also act as caregivers. We hypothesized that, among partners who were present during the ACE, those who were also present during (1) transportation to the hospital and (2) initial medical treatment would experience greater (a) anxiety early post-event and (b) posttraumatic stress symptoms (PSS) related to the event 4 months later. The associations between partner presence with patient anxiety and PSS were also explored. Methods: Participants were ACE patients and their partners recruited between March 2015 and December 2016 from the Intensive Cardiac Care Unit (ICCU) of the Sheba Medical Center in Israel (N = 143; all patients were males and partners were females). Partners self-reported whether or not they were present during the cardiac event, the hospital drive, and initial care. Patients and partners self-reported anxiety in-hospital and PSS, keyed to the ACE, an average of 4 months later. Data were analyzed using General Estimating Equations (GEE) and Multilevel Modeling. Results: Neither patient anxiety nor PSS differed according to partner presence during the drive to the hospital. In contrast, partners had higher anxiety when they were not present at all (difference = 3.65, p = 0.019) and when present during the event and during the drive (difference = 2.93, p = 0.029) as compared to when they were present for the event but not for the drive. Partners who were present during the event, but not the drive, had lower PSS than those who were present for both the event and the drive (difference = −4.64, p = 0.026). Conclusions: Partners who accompany patients on the drive to the hospital may inadvertently put themselves at risk for greater distress following their loved one’s cardiac event. Future research should enroll couples in an acute care context to inform couple-targeted tailored interventions to reduce distress in patients and their caregiving partners.

// Eran Kalmanovich 1, * , Alex Blatt 1, * , Svetlana Brener 1 , Meital Shlezinger 2 , Nir Shlomo 2 , Zvi Vered 1 , Hanoch Hod 2 , Ilan Goldenberg 2 and Gabby Elbaz-Greener 1 1 Department of Cardiology, Assaf Harofeh Medical Center, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel 2 The Heart Center, Chaim Sheba Medical Center, Tel Hashomer, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel * These authors have contributed equally to this work Correspondence to: Eran Kalmanovich, email: kalmanovicheran@gmail.com Keywords: cardiogenic shock, acute coronary syndrome, acute coronary syndrome Israeli surveys (ACSIS) Received: September 06, 2016 Accepted: February 27, 2017 Published: April 17, 2017 ABSTRACT Registries and other cohorts have demonstrated that early revascularization improve the survival of patients presenting with Cardiogenic Shock (CS) completing Aute coronary syndrome (ACS). Our aim was to describe the change in the clinical characteristics of these patients and their management and their outcome. The study population comprised 224 patients who were admitted with ACS complicated by cardiogenic shock who were enrolled in the prospective biannual Acute Coronary Syndrome Israeli Surveys (ACSIS) between 2000 and 2013 (1.7% of all patients admitted with ACS during the study period). Survey periods were categorized as early (years 2000-2004) and late (year 2006-2013). The rate of cardiogenic shock complicated ACS declined from 1.8% between the years 2000-2004 to 1.5% during the years 2006-2013. The clinical presentation in both the early and late groups was similar. During the index hospitalization primary percutaneous coronary intervention (PPCI) was more frequently employed during the late surveys [31% vs. 58% (p

In this Data in Brief article, we provide data of the cohort and statistical methods of the research- “Incidental abnormal ECG findings and long-term cardiovascular morbidity and all-cause mortality: a population based prospective study” (Goldman et al., 2019). Extended description of statistical analysis as well as data of cohort baseline characteristics and baseline ECG incidental abnormal findings of 2601 Israeli men and women without known cardiovascular disease (CVD) is presented. The cohort is part of the Israel study of Glucose Intolerance, Obesity and Hypertension (GOH) (Dankner et al., 2007). Furthermore, we provide the data on the performance assessment of the 23 - year CVD-risk and the 31- year all-cause mortality prediction models, which includes Receiver Operating Characteristic (ROC) curves, reclassification-based measures and calibration curve. Keywords: Electrocardiogram (ECG), Cardiovascular diseases, Cumulative incidence, Risk factors, Risk prediction, Survival analysis, Screening

Patients with non-ST elevation myocardial infarction who are managed noninvasively at presentation or are catheterized but without revascularization represent a heterogeneous and understudied population. We evaluated the clinical characteristics, management strategies, and outcomes of patients with non-ST elevation myocardial infarction (NSTEMI) who were enrolled in the prospective biannual Acute Coronary Syndrome Israeli Surveys from 2004 to 2013. Patients were divided into 3 groups: no catheterization (no angio), catheterization with revascularization (angio-revascularized), and catheterization without revascularization (angio-nonrevascularized) groups. The study included 3,198 patients with NSTEMI. Coronary angiography was performed in 2,525 (79%) during the index hospitalization, of whom 1899 (59%) underwent revascularization. Evidence-based therapies were administered during the index hospitalization at a significantly higher rate to those in the angio-revascularized group compared with the other 2 groups. Multivariate analysis showed that compared with those in the angio-revascularized and angio-nonrevascularized groups, patients in the no angio group experienced a significantly higher risk for 1-year mortality (hazard ratio 2.04 [p ≤0.0001] and 1.21 [p = 0.01], respectively). The risk associated with no revascularized was consistent in each risk subset analyzed, including an older age, and increased creatinine levels. In conclusion, our data, from a large real-world contemporary experience, suggest that patients with NSTEMI who do not undergo coronary revascularization during the index hospitalization represent a greater risk and undertreated group with increased risk for long-term mortality.

It is well established that a patient's partner can be deeply affected by the traumatizing nature of the patient's illness. Yet, no study to date has focused on post-traumatic stress symptoms (PTSS) among partners of patients coping with an acute coronary syndrome (ACS). The current study's main aims were to address this gap and to evaluate cardiac disease-induced (CDI) PTSS prevalence in partners of patients who experienced ACS. Patients who experienced ACS and their partners were interviewed by telephone 2 to 6 months after patients' hospitalization. All patients and partners were screened for CDI-PTSS. Demographic and medical variables as well as partners' level of exposure to the cardiac event were assessed. Prevalence of CDI-PTSS was higher among partners than among patients. Partners' number of CDI-PTSS was not significantly associated with patients' number of CDI-PTSS or with any of the other explanatory factors measured, except for education level. The preliminary results that arose from the current study point to the vast number of individuals who must act as caregivers for their ill partners while having to cope with their own PTSS. Much effort should be channelled into integrating partners into cardiac recovery programmes. Copyright © 2016 John Wiley & Sons, Ltd.

About half of all patients with heart failure are diagnosed with heart failure preserved ejection fraction (HFpEF). Until now, studies have failed to show that medical treatment improves the prognosis of patients with HFpEF.To evaluate changes in exercise capacity of patients with HFpEF compared to those with heart failure with reduced ejection fraction (HFrEF) following an exercise training program.Patient data was retrieved from a multi-center registry of patients with heart failure who participated in a cardiac rehabilitation program. Patients underwent exercise testing and an echocardiogram prior to entering the program and were retested6 months later.Of 216 heart failure patients enrolled in the program, 170 were diagnosed with HFrEF and 46 (21%) with HFpEF. Patients with HFpEF had lower baseline exercise capacity compared to those with HFrEF. Participating in a 6 month exercise program resulted in significant and similar improvement in exercise performance of both HFpEF and HFrEF patients: an absolute metabolic equivalent (MET) change (1.45 METs in HFrEF patients vs. 1.1 in the HFpEF group, P = 0.3).An exercise training program resulted in similar improvement of exercise capacity in both HFpEF and HFrEF patients. An individualized, yet similarly structured, cardiac rehabilitation program may serve both heart failure groups, providing safety and efficacy.

HYPOTHESIS We aimed to describe the kinetics and associated prognostic implications of the cardiac troponin release curve after a primary percutaneous coronary intervention (PPCI) in patients presenting with ST-segment elevation myocardial infarction (STEMI). PATIENTS AND METHODS We prospectively determined, in a prespecified timely manner, serial cardiac troponin I levels and obtained clinical, ECG, and echocardiographic data from 175 consecutive patients hospitalized with STEMI who underwent PPCI. The median peak troponin levels and time until troponin peaking were determined. RESULTS The troponin elevation curve following PPCI was single peaked, with a median value measuring 715 times the upper normal limit and a median peaking time of 8 h. Later-peaking troponin levels were associated with a TIMI flow grade of 0/1 at the initiation of angiography and with lack of at least 70% regression in the ST-elevation on the first post-PPCI ECG. Higher peak values were similarly associated with these two parameters as well as with a lower blush score and with distal embolization during PPCI. Both higher peak values and later peaking of troponin were associated independently with higher occurrence of the combined adverse cardiovascular event outcomes consisting of death, congestive heart failure, and recurrent infarction. CONCLUSION The cardiac troponin elevation curve following PPCI for STEMI shows a single peak and is affected by the adequacy of myocardial reperfusion. This method can serve as a simple surrogate for risk stratification of patients with STEMI who undergo PPCI.

According to Edmondson's Enduring Somatic Threat (EST) Model of PTSD Due to Acute Life-Threatening Medical Events, the nature of PTSD in the context of illness may differ from the nature of “traditional” PTSD in that it includes future-oriented alongside past-related intrusive thoughts. Yet almost no empirical studies to date have assessed the putative future-oriented quality of cardiac–disease-induced PTSD (CDI-PTSD). In the current study, we assessed the hypothesized associations between CDI-PTSD and fear of illness progression (FoP) – a novel theoretical conceptualization of patients' future-related anxieties. We hypothesized that FoP would be positively associated with CDI-PTSD, and especially with its specific items of intrusive thoughts. Patients (N = 112) were interviewed three months post-hospitalization for an acute coronary event via use of the PSS-SR-5 (to assess PTSD symptomatology), the FoP-Q-SF (to assess fear of illness progression), and the HADS (to assess anxiety and depression levels). Results indicated a strong positive association between CDI-PTSD and FoP, even when controlling for anxiety and depression. As hypothesized, the concepts of CDI-PTSD and fear of illness progression were strongly associated both at the level of the clusters as well as at the level of the specific items. The current study provides an initial empirical validation of the EST Model, especially regarding the future-oriented nature of PTSD resulting from acute cardiovascular disease.

Memory T cells producing interferon (IFN)γ and expressing very late antigen-1 (VLA-1) integrin collagen receptors are found in carotid atherosclerotic plaques, suggesting their involvement in coronary artery disease (CAD) as well. To determine the role of VLA-1+ T cells in CAD percent of CD3+ T cells binding monoclonal antibodies (mAb) to VLA-1 in peripheral blood (PB), and in coronary plaque material aspirated during coronary arterography and arterial blood, were analyzed in a cohort of 117 patients with CAD and 34 controls without CAD. % VLA-1+ T cells in PB was 0.63 ± 0.09% in controls compared to 0.96 ± 0.95% in patients with CAD (p

High-post clopidogrel platelet reactivity in acute coronary syndrome (ACS) patients is associated with adverse outcomes and may be related to clopidogrel dosing. Clinical studies evaluating different clopidogrel doses have resulted in conflicting conclusions. Clopidogrel dosing regimens have evolved over time, enabling us to evaluate platelet reactivity in real-life ACS patients undergoing percutaneous coronary intervention and treated with three different clopidogrel doses. Platelet reactivity was assessed with light transmitted aggregometry on the third day post clopidogrel loading in 404 consecutive ACS patients. Of them, 198 were treated with a standard regimen (300 mg loading, 75 mg/day maintenance dose), 95 with a high loading regimen (600 mg loading, 75 mg/day maintenance dose) and 111 with a high loading/high maintenance regimen (600 mg loading, 150 mg/day maintenance). Compared with the standard regimen, the high loading regimen resulted in significantly lower mean platelet reactivity to adenosine diphosphate (ADP) with a lower proportion of patients exhibiting clopidogrel non-responsiveness (11% vs. 28%, p = 0.004). Compared with the high loading regimen, the high loading/high maintenance regimen resulted in significantly lower mean platelet reactivity to ADP, but without a further drop in the number of non-responders (8.1% vs. 11%, p = 0.16). In conclusion, greater overall inhibition can be achieved with higher loading and maintenance doses in ACS patients. However, despite high clopidogrel doses, a sizable proportion of patients remained "resistant" to the effects of clopidogrel.

SummaryPrior studies have demonstrated significant individual variability of platelet response to clopidogrel, which affects clinical outcome. In patients with stable coronary artery disease (CAD) smoking, diabetes mellitus, elevated body mass index and renal insufficiency, significantly impact response to clopidogrel. The determinants of platelet response to clopidogrel in patients with acute coronary syndrome are unknown. Adenosine diphosphate (ADP)-induced platelet aggregation (PA), hs C-reactive protein, platelet count and mean platelet volume (MPV) were determined 72 hours post clopidogrel loading in 276 consecutive acute myocardial infarction (AMI) patients. Patients with ADP-platelet aggregation ≥ 70% were considered to be clopidogrel non-responders. Eighty-four patients (30%) were clopidogrel non-responders and 192 (70%) were responders (ADP-induced PA: 81 ± 17% vs 49 ± 17%, respectively, p

Coronary computed tomographic angiography can detect nonobstructive atherosclerotic lesions that would not otherwise have been detected with functional cardiac imaging. Currently, limited data exist regarding the clinical significance of these lesions in patients with acute chest pain. The aim of our study was to examine the prognostic significance of these nonobstructive findings in a patient population presenting with acute chest pain. We evaluated 959 consecutive patients who underwent coronary computed tomographic angiography for investigation of acute chest pain. The patients were classified as having normal (n = 545), nonobstructive coronary artery disease (CAD; defined as any narrowing50% diameter stenosis; n = 312), or obstructive CAD (narrowing of ≥50% diameter stenosis; n = 65). Follow-up data for a minimum of 12 months (mean 27 ± 11) was obtained for any major adverse coronary events consisting of death, nonfatal acute coronary syndrome, and coronary revascularization. Compared to patients with normal coronary arteries, those with nonobstructive CAD were older and had a greater prevalence of CAD risk factors. The incidence of major adverse coronary events was equally low among both these groups (0.6% vs 1.3%, for the normal and nonobstructive groups, respectively, p = 0.2). In conclusion, patients with either nonobstructive CAD or normal findings, as evaluated by coronary computed tomographic angiography, for acute chest pain during an intermediate-term follow-up period had equally benign clinical outcomes.

Partners' support has been associated with both patients' increased and decreased inclination toward health-promoting behaviors. Our hypothesis for understanding this enigma is that it is the interplay between partners' manner of care provision and patients' ability to accept these care efforts that may best predict patients' adherence. Thus, the current study's main goal was to examine the contribution of the interaction between caregivers' support style (sensitive and compulsive) and cardiac patients' sense of relational entitlement (restricted, excessive, assertive, entitlement expectations) to patients' medication adherence. The Adult Caregiving Questionnaire, the Sense of Relational Entitlement Scale, and the Medication Adherence Report Scale were administered to 114 cardiac patients and their partners, during patients' hospitalizations and 6 months later. The lowest levels of medication adherence were detected among patients high on restricted entitlement who were married to partners high on compulsive caregiving style. These findings strengthen our claim that it is the interaction between recipients' personality and providers' support style which explain self-regulatory processes that arise during times of family medical crises. (PsycINFO Database Record

Patients with stable coronary disease who exhibit platelet hypo-responsiveness to aspirin (ASA) have worse outcomes. Little data exist regarding platelet response to ASA in ST-elevation myocardial infarction (STEMI) patients. Our objective was to assess acute platelet response to ASA loading in STEMI patients undergoing primary percutaneous coronary intervention (PCI). The study comprised 102 consecutive patients with STEMI. All patients received a loading dose of 300 mg chewable ASA upon admission. Platelet reactivity was assessed immediately prior to primary PCI, at a median of 95(63 139) minutes after ASA loading. A bimodal response to arachidonic acid (AA) stimulation was observed, such that two distinct populations could be discerned: "good responders" had a mean AA-induced platelet aggregation of 36 ± 11% vs. 79 ± 9% for "poor responders." Despite equivalent demographic, clinical, and angiographic characteristics, good responders were significantly more likely to demonstrate early ST-segment resolution ≥70% after primary PCI (80% vs. 48%, p = 0.001), suggestive of better myocardial reperfusion. Early inhibition of AA-induced platelet aggregation post-ASA loading in the setting of STEMI is associated with better tissue reperfusion; however, a sizeable proportion of patients do not achieve significant inhibition of AA-induced platelet aggregation in response to ASA loading at the time of primary PCI.

Background: Anticoagulation with heparin is recommended in patients with an intra-aortic balloon pump (IABP) to prevent thrombosis and embolization. However, anticoagulation increases the risk of bleeding, particularly in the early postoperative period after cardiac surgery. We investigated the safety of heparin-free management after IABP insertion in patients who underwent cardiac surgery. Methods: We studied 203 consecutive patients who received perioperative IABP support between August 2004 and December 2011. All patients were managed without heparin and were followed for thrombotic and/or hemorrhagic complications. Results: Patients were divided into two groups, according to time of IABP treatment following surgery. Group I, 81 patients (39.9%) were treated less than 24 hours following surgery and Group II, 122 patients (60.1%) were treated more than 24 hours following surgery. Vascular complications developed in seven patients (3.4%), two in Group I and five in Group II. Three patients had major and four had minor limb ischemia. There were no major bleeding complications, but minor bleeding complications were observed in eight patients (4.2%). Conclusion: In patients undergoing cardiac surgery with IABP support, the rate of thromboembolic complications was relatively low compared to historical controls. Heparin-free management may reduce the risk of hemorrhagic complications, with a low risk of thrombotic complications. Heparin should not be routinely used in patients requiring IABP after cardiac surgery. (J Card Surg 2012;27:434-437)

Aims Multi-detector computed tomography (MDCT) has emerged as an efficient tool for detection of obstructive coronary artery disease (CAD) and assessment of patients with acute chest pain. MDCT may detect premature, non-obstructive atherosclerotic lesions which otherwise would have not been detected upon functional cardiac imaging tests. Currently, there is scarce data regarding the clinical significance of these lesions. The purpose of this study was to prospectively analyse the intermediate term outcome of patients admitted to chest pain unit (CPU) with findings of non-obstructive CAD upon MDCT. Method and results The study comprised 444 patients admitted to the CPU at Sheba Medical Center and underwent evaluation by MDCT for complaints of acute chest pain. Studies were classified as: normal; non-obstructive CAD (defined as any narrowing

Platelet activation occurs in an endothelium-dependent flow-mediated dilation (FMD) impairment environment. The aim of this study was to explore the association between platelet reactivity and brachial artery FMD in individuals without established cardiovascular disease (controls) and acute myocardial infarction (AMI) patients. We prospectively assessed brachial artery FMD in 151 consecutive subjects, 104 (69%) controls, and 47 (31%) AMI patients; 115 (76%) men, mean age 53 ± 11 years. Following overnight fasting and discontinuation of all medications for ≥ 12 h, percent change in brachial artery FMD (%FMD) and endothelium-independent, nitroglycerin-mediated vasodilation (%NTG) were assessed. Platelet aggregation was assessed by conventional aggregometry, and platelet adhesion and aggregation under flow conditions by cone-and-plate(let) technology (Impact-R). Smoking, diabetes, and hypertension were more common in AMI compared to control subjects (p

Mild therapeutic hypothermia has proved beneficial after out-of-hospital cardiac arrest in the adult population, when the initial rhythm is ventricular fibrillation (VF). In this study, data from 110 consecutive patients with out-of-hospital cardiac arrest due to VF (n = 86) or to non-VF rhythm (n = 24), admitted to an intensive cardiac care unit with restoration of spontaneous circulation and who remained unconscious on admission, were analyzed. Patients were cooled using an external cooling system. Of the patients with VF, 66% had favorable outcomes (Glasgow-Pittsburgh Cerebral Performance Category 1 or 2), and 30% died. Of the patients with non-VF, 8% had favorable outcomes (p

Statins confer an antiplatelet effect in hypercholesterolemic subjects and in stable coronary artery disease patients. We explored the antiplatelet effects of statins in ST-elevation myocardial infarction (STEMI) patients undergoing primary angioplasty. Of 120 STEMI patients, 80 (67%) received statins while 40 (33%) did not. Ex vivo platelet reactivity was studied on admission and 72 hours later by conventional aggregometry and under flow conditions (Impact R). Measures of platelet reactivity under flow conditions included aggregate size and surface coverage, signifying platelet aggregation and adhesion respectively. The effect of statins on platelet function under flow conditions and platelet aggregation was studied in?vitro in platelets from 10 STEMI patients. Platelets from each patient were incubated in?vitro with lovastatin or PBS as a control. The effect of lovastatin in the presence of a nitric oxide synthase inhibitor (L-NMMA) was also studied. Patients treated with statins were compared with those who did not have significantly lower ADP-induced platelet aggregation on the 4th day (56 ± 18% vs. 64 ± 17%, p=0.02). Platelet deposition under flow conditions as measured by surface coverage was reduced from admission to 72 hours later among statin-treated patients (19 ± 28% reduction, p

Acute coronary syndrome (ACS) is associated with activation of platelets and the coagulation system which could influence the incidence of early stent thrombosis (EST). We aimed to determine the incidence and predictors of EST in patients undergoing coronary stenting during ACS.The study comprised 1202 consecutive patients, drawn from a nationwide ACS survey, who underwent coronary stenting during ACS and were followed up for 30 days. Early stent thrombosis was based on the Academic Research Consortium definition.Thirty patients (2.5%) sustained EST. The occurrence of EST in patients with unstable angina/non-ST-elevation myocardial infarction and ST-elevation myocardial infarction (STEMI) was 0.9% and 3.9%, respectively (P.05), and was even higher (5.2%) in STEMI patients who underwent primary percutaneous coronary intervention. On multivariate analysis, STEMI (OR 6.3, 95% CI 2.1-18, P = .0008), multivessel disease (OR 5.9, 95% CI 1.9-21, P = .003) and Killip class/=2 (OR 2.9, 95% CI 1.3-6.6, P = .008) were independent correlates of EST. The use of bare versus drug-eluting stents was not associated with any significant difference in EST.Patients presenting with STEMI who are hemodynamically unstable and have multivessel coronary disease undergoing coronary stenting during ACS, are at increased risk of EST.

We evaluated the effect and optimal dose of clopidogrel pretreatment in patients with ST-elevation myocardial infarction undergoing primary percutaneous coronary intervention (PPCI). The study included 383 consecutive patients with ST-elevation myocardial infarction who had undergone PPCI and were prospectively followed up for a prespecified primary end point of recurrent acute coronary syndrome, stent thrombosis, congestive heart failure, and/or death at 30 days. Of these patients, 217 (57%) received clopidogrel loading before and 166 (43%) after PPCI. A similar number received low (300 mg) and high (600 mg) clopidogrel doses before and after PPCI. Clopidogrel loading before, compared with after, PPCI was associated with a lower incidence of the primary end point (21.7% vs 33.7%, p = 0.008). Clopidogrel pretreatment remained a significant predictor of the primary outcome after adjusting for potential confounders (odds ratio 0.54, 95% confidence interval 0.42 to 0.91). When patients were further stratified into 4 groups according to the timing and dosage of clopidogrel loading, the incidence of the primary outcome was 16% and 27% in those receiving 600 and 300 mg before and 28% and 39% in those receiving 600 and 300 mg after PPCI, respectively (p for trend

Background Anticoagulation with heparin is recommended with intra-aortic balloon pump (IABP) to prevent thrombosis and embolization. However, anticoagulation increases the risk of bleeding, particularly in combination with glycoprotein (GP) IIb/IIIa antagonists. Hypothesis We investigated the safety of using GP IIb/IIIa antagonists without heparin after IABP insertion in patients who underwent primary percutaneous coronary intervention (PCI). Methods Consecutive patients with acute myocardial infarction (AMI), who underwent primary PCI and were treated with GP IIb/IIIa antagonists without concomitant heparin, and in whom IABP was inserted, were followed during hospitalization for thrombotic and hemorrhagic complications. Results Ninety-seven patients were included in this analysis. Glycoprotein IIb/IIIa antagonist treatment duration was 12–24 h in 89% of patients, and IABP duration was up to 48 h in 97% of patients. Three patients (3.1%) developed vascular complications: 1 had a major limb ischemia (long IABP treatment), 1 had a minor limb ischemia, and 1 had a cerebrovascular event (after prolonged resuscitation). All patients were already on heparin at the time of the thrombotic events. The rates of major and minor bleeding complications were 9% and 15.5%, respectively. Conclusions The rate of thrombotic complications is relatively low in post-primary PCI patients with IABP treated with GP IIb/IIIa antagonists without concomitant heparin therapy. Such an approach may reduce the risk of hemorrhagic complications, with low risk of thrombotic complications. Copyright © 2009 Wiley Periodicals, Inc.

The diagnosis of acute myocarditis is challenging. Nonspecific clinical presentation and an overlap with the diagnosis of acute myocardial infarction present a diagnostic dilemma. The purpose of this article is to describe the role of cardiac MRI and transthoracic echocardiography (TTE) in the diagnosis of acute myocarditis.Thirty-two sequential patients (all male; average age, 33 years) with clinically suspected myocarditis were included. All patients underwent cardiac MRI with sequences dedicated for the evaluation of myocardial delayed enhancement and TTE for the evaluation of wall motion abnormalities (WMAs). Nine patients were excluded because of diagnosis of acute myocardial infarction (n=2) or inadequate cardiac MRI technique (n=7). Retrospective analysis of the images of the remaining 23 patients was performed.An epicardial pattern of abnormal patchy myocardial delayed enhancement was seen on cardiac MRI in 21 of 23 (91%) patients. WMAs were seen on TTE in eight of 23 (35%) patients. Regional rather than global involvement was seen mainly in the inferolateral segments, with a predominance in the midventricular portion.Cardiac MRI might have a greater impact than TTE in confirming the presence of acute myocarditis and evaluating the extent of myocardial involvement. Cardiac MRI provides noninvasive imaging that may obviate invasive procedures such as coronary catheter angiography or endomyocardial biopsy.

The aim of this study was to characterize the abnormalities in glucose homeostasis in intensive care unit patients following an acute coronary event. The study population included all non-diabetic patients ages 20-80 years that were admitted to a coronary intensive unit. Glucose, insulin and C-peptide levels during an oral glucose tolerance test (OGTT) were measured during the acute admission. From January to September 2003, 277 patients were admitted to the coronary unit. Of these, 127 patients underwent an OGTT. Of these, only 29 patients (23%) exhibited normal glucose metabolism. The remainder had type 2 diabetes (32%), impaired glucose tolerance (37%) or isolated impaired fasting glucose (8%, 100-125 mg/dl). Based on homeostasis model assessment (HOMA) calculations, diabetic patients had impaired beta-cell function and patients with elevated fasting glucose levels were insulin resistant. Beta-cell dysfunction during the acute stress seems to contribute to the glucose abnormalities. Most patients who experience an acute coronary event demonstrate abnormal glucose metabolism. Post glucose-load abnormalities are more common than abnormal fasting glucose level in this situation. It is postulated that the acute stress of a coronary event may contribute to the dysglycemia.

Whether increasing doses of clopidogrel can overcome nonresponsiveness was evaluated. Clopidogrel nonresponsiveness was found in up to 25% of treated patients and was associated with worse prognosis in patients with acute coronary syndrome and patients undergoing coronary intervention. Adenosine diphosphate (ADP)-induced platelet aggregation was prospectively determined on day 4 of acute myocardial infarction in 200 consecutive patients, who received clopidogrel 300 mg as a loading dose and 75 mg/day thereafter. Thirty patients (15%) had ADP-induced platelet aggregationor=80% using light transmittance aggregometry and were considered clopidogrel nonresponders. Nonresponders were reloaded with clopidogrel 600 mg, followed by 150 mg/day for 4 weeks. A 75-mg/day dose was resumed thereafter. ADP-induced platelet aggregation was reassessed 4 hours after reloading and biweekly for 10 weeks. Flow cytometry was used to determine platelet P-selectin expression and fibrinogen binding before and 4 hours after reloading. ADP-induced platelet aggregation significantly decreased 4 hours after reloading (from 83 +/- 6% to 56 +/- 14%; p0.01). The decrease in platelet aggregation was maintained throughout the 4-week doubled maintenance dose. After resuming a maintenance dose of 75 mg/day, ADP-induced platelet aggregation returned to 66 +/- 12% (p0.001), and 5 patients (17%) had ADP-induced platelet aggregationor=80%. Flow cytometry showed a significant decrease in P-selectin expression (from 37 +/- 16% to 26 +/- 13%; p0.01) and fibrinogen binding (from 84 +/- 7% to 70 +/- 13%; p0.01) in ADP-stimulated platelets 4 hours after reloading. In conclusion, clopidogrel reloading and increased maintenance dose may overcome clopidogrel nonresponsiveness in patients with acute myocardial infarction.

Unresponsiveness to clopidogrel or aspirin has been reported in patients with acute coronary syndrome (ACS). Platelet aggregometry (PA) and the Impact-R [Cone and Plate(let) Analyzer (CPA) technology, measuring whole blood platelet adhesion under flow conditions] were compared in detecting laboratory unresponsiveness to clopidogrel and aspirin among ACS patients. Platelet-rich plasma (PRP) samples were evaluated in 404 patients by PA using adenosine diphosphate (ADP) and arachidonic acid (AA) and whole blood samples by the Impact-R ADP- and AA-response tests. The first cohort (n=114) was assayed by PA on days 1 and 4 of the onset of ACS. A patient with relative decrease of/=10% in ADP-induced maximal platelet aggregation after clopidogrel treatment was defined as laboratory non-responding (NR) patient to clopidogrel. This relative value correlated well with an absolute value of ADP-induced aggregation/=70%. A patient with an absolute value of AA-induced maximal aggregation/=60% was defined as laboratory NR patient to aspirin. The second cohort (n=290) was tested on day 4 by both systems and results analyzed by receiver operating characteristic curve. The following cut-off values of the Impact-R surface coverage were obtained:/=2.8% and/=3.4% for clopidogrel and aspirin NR patients, respectively. The incidence of NR patients to clopidogrel and aspirin, according to the two methods was 27% and 22%, respectively. Impact-R compared to PA in detecting clopidogrel and aspirin NR patients revealed: 79% and 82% agreement, 71% and 73% sensitivity, 83% and 86% specificity, respectively. In conclusion, the Impact-R and PA results demonstrated high degree of similarity.

Background— The increasing use of higher-than-approved doses of clopidogrel in clinical practice is based in part on the desire for greater levels of inhibition of platelet aggregation (IPA). Prasugrel is a new thienopyridine that is more potent than standard-dose clopidogrel in healthy subjects and patients with stable coronary artery disease. The relative antiplatelet effects of prasugrel versus high-dose clopidogrel in percutaneous coronary intervention patients are unknown. Methods and Results— Prasugrel in Comparison to Clopidogrel for Inhibition of Platelet Activation and Aggregation–Thrombolysis in Myocardial Infarction 44 (PRINCIPLE-TIMI 44) was a randomized, double-blind, 2-phase crossover study of prasugrel compared with high-dose clopidogrel in patients undergoing cardiac catheterization for planned percutaneous coronary intervention. The primary end point of the loading-dose phase (prasugrel 60 mg versus clopidogrel 600 mg) was IPA with 20 μmol/L ADP at 6 hours. Patients with percutaneous coronary intervention entered the maintenance-dose phase, a 28-day crossover comparison of prasugrel 10 mg/d versus clopidogrel 150 mg/d with a primary end point of IPA after 14 days of either drug. In this study, 201 subjects were randomized. IPA at 6 hours was significantly higher in subjects receiving prasugrel (mean±SD, 74.8±13.0%) compared with clopidogrel (31.8±21.1%; P P Conclusions— Among patients undergoing cardiac catheterization with planned percutaneous coronary intervention, loading with 60 mg prasugrel resulted in greater platelet inhibition than a 600-mg clopidogrel loading dose. Maintenance therapy with prasugrel 10 mg/d resulted in a greater antiplatelet effect than 150 mg/d clopidogrel.

Objectives: External counter pulsation therapy (ECPT) offers symptomatic relief and improves ischemia in patients with refractory angina pectoris. We aimed to determine the effects of ECPT on circulating endothelial progenitor cells (EPCs). Methods: We prospectively studied 25 patients with angina pectoris treated with ECPT (n = 15) or receiving standard care (n = 10). The number of EPCs positive for CD34 and kinase insert domain receptor (KDR) was determined by flow cytometry and the number of colony-forming units (CFUs) was assessed in a 7-day culture, before ECPT and after 9 weeks. Results: ECPT improved anginal score from a median of 3.0 to 2.0 (p < 0.001). Concomitantly, ECPT increased EPC number from a median of 10.2 to 17.8/105 mononuclear cells (p < 0.05), and CFUs from 3.5 to 11.0 (p = 0.01). Flow-mediated dilatation was improved by ECPT from 7.4 to 12.2% (p < 0.001) and correlated with EPC-CFUs (r = 0.461, p = 0.027). The levels of asymmetric dimethylarginine were reduced by ECPT from 0.70 to 0.60 µmol/l (p < 0.01). In contrast, the same parameters did not change in the control group, before and after follow-up. Conclusions: The present pilot study shows, for the first time, that ECPT is associated with increased number and colony-forming capacity of circulating EPCs.

Myocardial infarction is a major cause of death and disability worldwide. Coronary atherosclerosis is a chronic disease with stable and unstable periods. During unstable periods with activated inflammation in the vascular wall, patients may develop a myocardial infarction. Myocardial infarction may be a minor event in a lifelong chronic disease, it may even go undetected, but it may also be a major catastrophic event leading to sudden death or severe hemodynamic deterioration. A myocardial infarction may be the first manifestation of coronary artery disease, or it may occur, repeatedly, in patients with established disease. Information on myocardial infarction attack rates can provide useful data regarding the burden of coronary artery disease within and across populations, especially if standardized data are collected in a manner that demonstrates the distinction between incident and recurrent events. From the epidemiological point of view, the incidence of myocardial infarction in a population can be used as a proxy for the prevalence of coronary artery disease in that population. Furthermore, the term myocardial infarction has major psychological and legal implications for the individual and society. It is an indicator of one of the leading health problems in the world, and it is an outcome measure in clinical trials and observational studies. With these perspectives, myocardial infarction may be defined from a number of different clinical, electrocardiographic, biochemical, imaging, and pathological characteristics. In the past, a general consensus existed for the clinical syndrome designated as myocardial infarction. In studies of disease prevalence, the World Health Organization (WHO) defined myocardial infarction from symptoms, ECG abnormalities, and enzymes. However, the development of more sensitive and specific serological biomarkers and precise imaging techniques allows detection of ever smaller amounts of myocardial necrosis. Accordingly, current clinical practice, health care delivery systems, as well as epidemiology and clinical trials all require a …

[Graphic][1] Myocardial infarction is a major cause of death and disability worldwide. Coronary atherosclerosis is a chronic disease with stable and unstable periods. During unstable periods with activated inflammation in the vascular wall, patients may develop a myocardial infarction. Myocardial infarction may be a minor event in a lifelong chronic disease, it may even go undetected, but it may also be a major catastrophic event leading to sudden death or severe haemodynamic deterioration. A myocardial infarction may be the first manifestation of coronary artery disease, or it may occur, repeatedly, in patients with established disease. Information on myocardial infarction attack rates can provide useful data regarding the burden of coronary artery disease within and across populations, especially if standardized data are collected in a manner that demonstrates the distinction between incident and recurrent events. From the epidemiological point of view, the incidence of myocardial infarction in a population can be used as a proxy for the prevalence of coronary artery disease in that population. Furthermore, the term myocardial infarction has major psychological and legal implications for the individual and society. It is an indicator of one of the leading health problems in the world, and it is an outcome measure in clinical trials and observational studies. With these perspectives, myocardial infarction may be defined from a number of different clinical, electrocardiographic, biochemical, imaging, and pathological characteristics. In the past, a general consensus existed for the clinical syndrome designated as myocardial infarction. In studies of disease prevalence, the World Health Organization (WHO) defined myocardial infarction from symptoms, ECG abnormalities, and enzymes. However, the development of more sensitive and specific serological biomarkers and precise imaging techniques allows detection of ever smaller amounts of myocardial necrosis. Accordingly, current clinical practice, health care delivery systems, as well as epidemiology and clinical trials all require a … [1]: /embed/inline-graphic-1.gif

Background/Aims: Physicians’ perception of antecedent physical/cognitive status may account for the suboptimal implementation of acute coronary syndrome (ACS) guidelines. Methods: In an ACS survey of all cardiac wards, physicians’ perception of antecedent physical/cognitive status was prospectively recorded and categorized as either normal, mildly impaired or significantly impaired. We examined the impact of antecedent status on the use of evidence-based medications and procedures and on mortality. Results: Of the 2,021 patients, 1,025 (51%) had ST elevation. Impaired antecedent physical/cognitive status was diagnosed in 417 patients (20.6%), more commonly among non-ST-elevation patients (26.2 vs. 15.2%). Patients with impaired physical/cognitive status, with or without ST elevation, had significantly worse baseline demographic and clinical characteristics. They less often received aspirin, clopidogrel, platelet glycoprotein IIb/IIIa receptor antagonists, statins and β-adrenergic blockers, and significantly less often underwent in-hospital catheterization and revascularization. Reperfusion treatment was given significantly less frequently to ST elevation patients with impaired status (63.0% for normal vs. 50.8% and 33.3% for mildly and significantly impaired status, respectively; p = 0.001). After adjustment for differences in baseline characteristics, impaired antecedent status remained independently associated with lower use of these therapies and higher mortality rates. Conclusions: ACS guideline implementation is significantly influenced by physicians’ perception of antecedent physical/cognitive status, and thus is a crucial parameter for understanding ACS management and outcomes.

Background— Ranolazine, a piperazine derivative, reduces ischemia via inhibition of the late phase of the inward sodium current (late I Na ) during cardiac repolarization, with a consequent reduction in intracellular sodium and calcium overload. Increased intracellular calcium leads to both mechanical dysfunction and electric instability. Ranolazine reduces proarrhythmic substrate and triggers such as early afterdepolarization in experimental models. However, the potential antiarrhythmic actions of ranolazine have yet to be demonstrated in humans. Methods and Results— The Metabolic Efficiency With Ranolazine for Less Ischemia in Non–ST-Elevation Acute Coronary Syndrome (MERLIN)–Thrombolysis in Myocardial Infarction (TIMI) 36 (MERLIN-TIMI 36) trial randomized 6560 patients hospitalized with a non–ST-elevation acute coronary syndrome to ranolazine or placebo in addition to standard therapy. Continuous ECG (Holter) recording was performed for the first 7 days after randomization. A prespecified set of arrhythmias were evaluated by a core laboratory blinded to treatment and outcomes. Of the 6560 patients in MERLIN-TIMI 36, 6351 (97%) had continuous ECG recordings that could be evaluated for arrhythmia analysis. Treatment with ranolazine resulted in significantly lower incidences of arrhythmias. Specifically, fewer patients had an episode of ventricular tachycardia lasting ≥8 beats (166 [5.3%] versus 265 [8.3%]; P P P =0.08). In addition, pauses ≥3 seconds were less frequent with ranolazine (97 [3.1%] versus 136 [4.3%]; P =0.01). Conclusions— Ranolazine, an inhibitor of late I Na , appears to have antiarrhythmic effects as assessed by continuous ECG monitoring of patients in the first week after admission for acute coronary syndrome. Studies specifically designed to evaluate the potential role of ranolazine as an antiarrhythmic agent are warranted.

Purpose The number of elderly patients with acute myocardial infarction (AMI) is growing rapidly, and their early and postdischarge mortality is high. Several studies have reported a decline in mortality after myocardial infarction; however, the magnitude of the decline among the elderly has not been fully investigated. Methods We assessed trends in management, in-hospital, and long-term outcomes of 1475 elderly patients (aged ≥75 years, 42% women) hospitalized with AMI in all 25 operating coronary care units in Israel between 1992 and 2002, from our prospective nationwide biennial surveys. Results Between 1992 and 2002, a significant increase was observed in the use of acute reperfusion therapy (27%-48%), coronary angiography (6%-47%), percutaneous coronary intervention (3%-33%), coronary bypass (2%-8%), aspirin (53%-88%), beta-blockers (18%-65%), angiotensin-converting enzyme inhibitors (26%-63%), and lipid-lowering drugs (0%-43%). These changes were associated with a 42% reduction in 30-day mortality (27.6%-16.1%; adjusted odds ratio 0.57; 95% confidence interval [CI], 0.36-0.93). One-year cumulative mortality declined by 20% (37%-29%; adjusted odds ratio 0.74; 95% CI, 0.49-1.13). Conclusions The management of elderly patients with AMI changed substantially during the last decade. This change was associated with a significant reduction in early mortality, whereas cumulative 1-year mortality improved only slightly. Better adherence to in-hospital management guidelines and better implementation of postdischarge health policy may further decrease mortality and morbidity in the elderly after AMI.

It is well established that a patient's partner can be deeply affected by the traumatizing nature of the patient's illness. Yet, no study to date has focused on post-traumatic stress symptoms (PTSS) among partners of patients coping with an acute coronary syndrome (ACS). The current study's main aims were to address this gap and to evaluate cardiac disease-induced (CDI) PTSS prevalence in partners of patients who experienced ACS. Patients who experienced ACS and their partners were interviewed by telephone 2 to 6 months after patients' hospitalization. All patients and partners were screened for CDI-PTSS. Demographic and medical variables as well as partners' level of exposure to the cardiac event were assessed. Prevalence of CDI-PTSS was higher among partners than among patients. Partners' number of CDI-PTSS was not significantly associated with patients' number of CDI-PTSS or with any of the other explanatory factors measured, except for education level. The preliminary results that arose from the current study point to the vast number of individuals who must act as caregivers for their ill partners while having to cope with their own PTSS. Much effort should be channelled into integrating partners into cardiac recovery programmes. Copyright © 2016 John WileySons, Ltd.

The prevalence of thrombophilia and dyslipidemia among young survivors of acute coronary syndrome has not been clearly defined. The purpose of the current study was to investigate the prevalence of multiple markers of thrombophilia and dyslipidemia in a cohort of consecutive young survivors of acute coronary syndrome. The study cohort included 156 consecutive young patients (men45 and women50 years), admitted to the intensive cardiac care unit with newly diagnosed acute coronary syndrome. Analysis included baseline, clinical and epidemiological characteristics, angiographic coronary anatomy, echocardiographic evaluation, extensive lipid and thrombophilia laboratory profiles, and in-hospital and 1-year clinical outcomes for all patients. Acute myocardial infarction was diagnosed in 142 (92 %) patients, of whom 108 (72 %) had ST-segment elevation. Eighteen (12 %) patients had no traditional risk factors. Low levels of high-density lipoprotein (40 mg/dL) were found in 101 (65 %) patients, and 49 (34 %) patients had elevated levels of lipoprotein(a) (Lp(a)) (30 mg/dL). Eighteen (12 %) patients were diagnosed with antiphospholipid antibody syndrome (APS), and 73 (47 %) had at least one laboratory finding consistent with thrombophilia. Patients with APS had significantly higher levels of Lp(a) (46 ± 32 vs. 29 ± 31 mg/dL, p = 0.005). APS is a common prothrombotic state found in young survivors of acute coronary syndrome. Lp(a) levels are elevated among APS patients who present with premature acute coronary syndrome.

Objectives: To investigate characteristics, management and outcome of patients with acute myocardial infarction (AMI) and chronic renal insufficiency (CRI). Background: Patients with AMI and CRI are considered to be at high risk of complications and death. Physicians may be reluctant to prescribe life-saving medications to patients with concomitant CRI. Methods: We compared clinical characteristics, management and outcome of 1,683 consecutive AMI patients in three categories of renal function: (1) normal renal function (3.5 mg/dl) (n = 47). Results: CRI patients were older and were more likely to have other co-morbidities such as hypertension, diabetes mellitus, prior AMI, stroke, angina and heart failure. Compared with patients with normal renal function, standard therapy for AMI including thrombolysis, aspirin, angiotensin-converting-enzyme inhibitors, β-blockers and lipid lowering agents was underutilized in CRI patients and these patients were more likely to have in-hospital complications such as heart failure, atrial or ventricular fibrillation, cardiogenic shock, sepsis, worsening of renal function and death within 30 days [odds ratio (OR) = 3.3; 95% confidence interval (CI) = 2.0–4.8]. After adjustment for age and co-morbidities, the association between mild to moderate CRI and 30-days mortality declined, whereas severe CRI remained an independent determinant of mortality (OR = 4.8; 95% CI = 2.0–11.4). Adjustment for aspirin, angiotensin-converting-enzyme inhibitors and β-blocker therapy weakened the association between CRI and death within 30 days after AMI. Conclusions: CRI patients are more likely to experience serious complications and death early after AMI. Underutilization of standard care, particularly β-blocker therapy, contributes to increased mortality risk in these patients.

Background: Although clopidogrel and aspirin (dual therapy, DT) are used for acute coronary syndrome (ACS), sometimes treatment with warfarin (triple therapy, TT) is required. Aim: To determine the incidence, complications, and outcomes of TT. Methods: We analyzed Israeli surveys of ACS from 2000 to 2004. Results: In these surveys, 5,706 (96%) were discharged alive from hospital. Post-ACS TT and DT were 76 patients (1.3%) and 2,661 patients (46.7%), respectively. The TT group was older with more prior cardiac disease. During hospitalization, the TT patients received more intravenous anticoagulant and antithrombotic agents, and had more heart failure, arrhythmias, ischemia, and major bleeding (2.6 vs. 0.6%, p = 0.03). There were no differences in adjusted 30-day and 6-month mortality between the 2 groups. Conclusion: TT is feasible among ACS patients who require concomitant warfarin treatment.

Heart Institute, Sheba Medical Center, Tel-Hashomer and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, IsraelSummaryBackground: Left ventricular apical ballooning, a new syn-drome recently described in Japan, is characterized by chestpain, electrocardiographic changes mimicking acute myocar-dial infarction, and transient apical dyskinesia with normalcoronary arteries. Although several studies have defined theclinical characteristics, the prevalence of this syndrome re-mains unclear. Hypothesis: This study sought to determine the prevalenceof left ventricular apical ballooning syndrome.Methods: From January 2002 to September 2004, clini-cal, echocardiographic, and angiographic data of hospital-ization and follow-up were collected from 638 consecutivepatients referred to our Heart Institute for primary percuta-neous intervention.Results: Thirteen patients (2%) were diagnosed with tran-sient left ventricular apical ballooning. All but one patientwere women, representing a 6% incidence for the female pa-tients with acute myocardial infarction. A triggering factorwas identified in eight. One patient died of cardiogenic shock.Left ventricular systolic function recovered completely within4–5 weeks in the remaining 12 survivors.Conclusion: This syndrome is not uncommon and shouldbe considered particularly in female patients presenting withacute myocardial infarction.Key words: coronary angiography, stress cardiomyopathy,apical ballooning, TakotsuboIntroductionRecent reports, initially from Japan, have described a syndrome characterized by chest pain, electrocardiographic(ECG) changes, transient left ventricular (LV) apical wall mo-tion abnormality, without any significant coronary artery dis-ease. Patients were usually women aged >50 years in whom atriggering event, mostly emotional distress, was identified.This condition has also been termed “Takotsubo-like LV dys-function” because of the peculiar shape seen on left ventricu-logram, which resembles a “tako-tsubo” pot (with a round bot-tom and narrow neck) used for trapping octopuses in Japan.

The benefit of rescue percutaneous coronary intervention (PCI) in acute myocardial infarction patients, who fail to show signs of reperfusion after full dose thrombolysis, is still an unresolved issue.To assess the outcomes of patients who underwent rescue PCI after full-dose thrombolytic therapy and compare them to patients treated only with thrombolysis in the Acute Coronary Syndrome Israel Surveys (ACSIS).ACSIS is a biannual survey on acute myocardial infarction performed in all 26 intensive cardiac care units in Israel during a two-month period. 2,018 patients were admitted with acute myocardial infarction during the two-month period in the 2000 and 2002 surveys, and 796 of them were treated with thrombolytic therapy.Rescue PCI was performed in 99 patients who failed to show signs of reperfusion. The control group consisted of patients with unsuccessful thrombolysis and no further intervention. Patients who underwent rescue PCI had a numerically higher incidence of anterior wall myocardial infarction, diabetes, higher Killip class on admission and cardiogenic shock. Furthermore, almost half of these patients had reduced left ventricular function (P = 0.03). During hospitalization, there was a significantly higher prevalence of recurrent ischemic events and major bleeding complications in patients who underwent rescue PCI. In-hospital, 30-day and one-year mortality rates were similar between the two groups. By multivariate analyses, Killip class 3-4 (OR: 2.62, CI = 0.95-6.58, P = 0.05) and streptokinase treatment (OR: 0.623, CI = 0.4-0.97, P = 0.05) were independent predictors of rescue PCI. Rescue angioplasty was associated with 15% risk-reduction (CI = 0.45-1.97, P = 0.05) in 30-day mortality and recurrent emergent hospitalization.Patients who underwent rescue PCI had similar short- and long-term mortality rates compared to patients treated with thrombolysis alone, despite differences in baseline characteristics. Rescue angioplasty was associated with a 15% risk reduction in mortality at 30-days, at the cost of higher rate of recurrent ischemic events and bleeding complications. Therefore, rescue angioplasty may be an equalizer in severely ill patients who receive thrombolytic therapy and fail to show signs of reperfusion.

ObjectivesThe aim of this study was to evaluate the significance of increased left atrial (LA) volume determined within the first 48 h of admission as a long-term predictor of outcome in patients with acute myocardial infarction (MI).BackgroundThe LA volume reflects left ventricular (LV) diastolic properties. Whereas other LV Doppler diastolic characteristics are influenced by acute changes in LV function, LA volume is stable and reflects diastolic properties before MI.MethodsClinical and echocardiographic parameters were prospectively collected in 395 consecutive patients with acute MI. Patients with LA volume index (LAVI) >32 ml/m2(normal + 2 standard deviations) were compared with those with LAVI ≤32 ml/m2. Independent clinical and echocardiographic prognostic risk factors for five years' mortality were determined by the Cox proportional hazard model.ResultsLeft atrial volume index >32 ml/m2was found in 63 patients (19%) who had a higher incidence of congestive heart failure on admission (24% vs. 12%, p < 0.01), a higher incidence of mitral regurgitation, increased LV dimensions, and reduced LV ejection fraction when compared with patients with LAVI ≤32 ml/m2. Their five-year mortality rate was 34.5% versus 14.2% (p < 0.001). Significant independent risk predictors of five years' mortality were age (10 years) (odds ratio [OR] 1.45; 95% confidence interval [CI]1.14 to 1.86), Killip class ≥2 on admission (OR 2.30; 95% CI 1.29 to 4.09), LAVI >32 ml/m2(OR 2.22; 95% CI 1.25 to 3.96), diabetes (OR 1.94; 95% CI 1.15 to 3.28), and LV restrictive filling pattern (OR 1.89; 95% CI 1.09 to 3.31).ConclusionsIn patients with acute MI, increased LA volume, determined within the first 48 h of admission, is an independent predictor of five-year mortality with incremental prognostic information to clinical and echocardiographic data.

Right bundle branch block and complete atrioventricular (AV) block are conduction disorders (CDs) that have been observed in 14% of patients admitted with ST-elevation acute myocardial infarction. CDs carry a poor prognosis, with a threefold increase in the mortality rate, mainly due to cardiogenic shock and recurrent fatal myocardial infarction at 1-year follow-up. According to multivariable analysis, CD was the second strongest predictor of death, after high Killip class. Compared with patients without CD, the 1-year outcome of patients with CD was identically worse, irrespective of whether CD appeared during admission, disappeared, or remained constant. Similar adverse outcomes were seen in patients with complete AV block and right bundle branch block.

I 1963, Burch et al 1,2 reasoned that infarction of a papillary muscle causing failure to contract during ventricular ejection would result in mitral valve prolapse during the latter half of systole. This concept was developed to explain the timing of the murmur observed in ischemic mitral regurgitation (MR), which is frequently midto late systolic. However, experimentally induced isolated papillary muscle damage, ischemia, and infarction have repeatedly failed to produce MR. Also, MR caused by prolapse is not observed clinically in acute myocardial infarction or ischemia. Instead, similar to functional MR in idiopathic dilated cardiomyopathy, the mitral leaflets have been found to be apically displaced, showing incomplete leaflet closure. This has been attributed to dyskinesia or distortion of the region of the left ventricle from which the papillary muscles arise, displacing the papillary muscles and thus restricting leaflet closure. Nevertheless, the theory of papillary muscle dysfunction causing prolapse has survived even into recent editions of cardiology textbooks. One of the reasons may be the lack of an alternative explanation for the late systolic murmur in ischemic MR. Such an explanation may be found in the pattern of phasic regurgitant orifice area variation during systole, which reflects the underlying mechanism of MR. In idiopathic dilated cardiomyopathy, echocardiographic recordings of the proximal flow convergence region during MR have demonstrated a distinct biphasic pattern of flow and orifice area variation: a decrease during left ventricular contraction, an increase during ventricular relaxation. We hypothesized that the pattern of regurgitant orifice area variation in ischemic MR due to inferoposterior wall motion abnormalities will be similar, because the observed geometric substrate of regurgitation—apical tenting of the mitral valve—suggests a similar mechanism. In particular, we sought to demonstrate that the phenomenon of late systolic murmur can be explained by a late systolic increase in regurgitant orifice area and flow, a variant of the biphasic pattern of functional MR, and that it is related to mitral leaflet tethering and not mitral valve prolapse.

Unlike thrombolytic agents, there are conflicting data regarding the time-dependent effect of aspirin treatment on outcome in acute myocardial infarction (AMI). We sought to evaluate the impact of timing of aspirin administration (before vs after thrombolysis) on mortality of patients with AMI. Our study included 1,200 patients with ST elevation AMI treated with thrombolysis. Early (n = 364) versus late (n = 836) users were defined as those receiving emergency aspirin before versus after initiation of thrombolysis, respectively. Time (median) from symptom onset to initiation of aspirin treatment was significantly shorter in early versus late users (1.6 vs 3.5 hours; p0.001). There were no significant differences between the 2 groups with respect to baseline clinical characteristics. Early aspirin users were more likely to develop reischemia, to be treated with beta blockers, to be referred to coronary angiography, percutaneous transluminal coronary angioplasty, or coronary artery bypass graft surgery. Early users experienced lower mortality at 7 days (2.5% vs 6.0%, p = 0.01), 30 days (3.3% vs 7.3%, p = 0.008), and 1 year (5.0% vs 10.6%, p = 0.002) than late users. This survival benefit persisted for patients with and without previous aspirin therapy or revascularization and after adjustment for baseline characteristics and therapies at 7 days (odds ratio 0.36, 95% confidence interval 0.15 to 0.79), at 30 days (odds ratio 0.39, 95% confidence interval 0.17 to 0.82), and at 1 year (odds ratio 0.41, 95% confidence interval 0.21 to 0.74). Our study proposes a time-dependent benefit from aspirin in patients with AMI treated with thrombolysis.