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Background Possible ethnic differences in clinical characteristics and long-term prognosis of contemporary patients with vasospastic angina (VSA) remain to be elucidated. Methods and results The Japanese Coronary Spasm Association (JCSA) conducted an international, prospective, and multicenter registry study for VSA patients. A total of 1457 VSA patients (Japanese/Caucasians, 1339/118) were enrolled based on the same diagnostic criteria. Compared with Caucasian patients, Japanese patients were characterized by higher proportions of males (68 vs. 51%) and smoking history (60 vs. 49%). Japanese patients more often had angina especially during the night and early morning hours, compared with Caucasians. Ninety-five percent of Japanese and 84% of Caucasian patients underwent pharmacological provocation test. Importantly, no significant differences in the patterns of coronary spasm were apparent, with diffuse spasm most frequently noted in both ethnicities. The prescription rate of calcium-channel blockers was higher in Japanese (96 vs. 86%), whereas the uses of nitrates (46 vs. 59%), statins (43 vs. 65%), renin-angiotensin-system inhibitors (27 vs. 51%), and β-blockers (10 vs. 24%) were more common in Caucasian patients. Survival rate free from major adverse cardiac events (MACE) was slightly but significantly higher in Japanese than in Caucasians (86.7 vs. 76.6% at 5 years, P Conclusion These results indicate that there are ethnic differences in clinical profiles and long-term prognosis of contemporary VSA patients.

Ivabradine is a heart rate reducing agent that exhibits anti-ischemic effects through the inhibition of funny electrical current in the sinus node resulting in heart rate reduction, thus enabling longer diastolic perfusion time, and reduced myocardial oxygen consumption without detrimental changes in arterial blood pressure, coronary vasomotion, and ventricular contractility. The current guideline-based clinical use of Ivabradine is reserved for patients with stable angina pectoris who cannot tolerate or whose symptoms are inadequately controlled with beta blockers. In patients with chronic heart failure and reduced ejection fraction, Ivabradine has demonstrated beneficial effects in improving clinical outcomes when added to conventional therapy. However, the role of Ivabradine in acute coronary syndromes has not been established. Based on the results from some relevant preclinical studies and a limited amount of clinical data that were reported recently, the role of Ivabradine in acute ischemic events warrants further investigation. The aim of this review is to provide an overview of the available literature on the potential role of Ivabradine in the clinical context of acute coronary syndromes.

Background The presence of late gadolinium enhancement (LGE) at cardiac magnetic resonance (CMR) has diagnostic and prognostic value in patients with acute myocarditis (AM). Aim of our study was to quantify the changes in LGE extension (LGE%) early after AM and evaluate its relations with biventricular function and morphology. Methods We investigated 76 consecutive patients with AM (acute onset of chest pain/heart failure/ventricular arrhythmias not explained by other causes, and raised troponin) that met CMR criteria based on myocardial oedema at T2-weighted images and LGE on post-contrast images at median time of 6 days from onset of symptoms. We quantified LGE% at baseline and after 148 days in 49 patients. Results Median left ventricular (LV)-ejection fraction (EF) was 64% (interquartile range [Q1–Q3]: 56–67%), and LGE% 9.4% (Q1–Q3: 7.5–13.2%). LGE% was correlated with LV end-systolic volume index (LV-ESVi; r = + 0.34; p = 0.003). LGE% was inversely correlated with LV-EF (r = − 0.31; p = 0.009) and time to CMR scan (r = − 0.25; p = 0.028). In the 49 patients with a second CMR scan, despite no significant variations in LV-EF, a significant decrease of LGE% was observed (p < 0.0001) with a relative reduction of 42% compared with baseline. Patients showing increased LV-ESVi at follow up had a lower decrease of LGE% (p = 0.038). Conclusions In the acute phase of AM the LGE extension is a dynamic process that reflects impairment of LV function and is time dependent. LGE% appears one of the CMR parameters with the largest relative variations in the first months after AM

Impella RP has been used to treat right ventricular failure (RVF) developing in various clinical settings that underlay different pathological mechanisms and lead to distinct prognostic implications.This is a single-centre retrospective study including all consecutive patients, from January 2015 to December 2018, with inferior STEMI due to acute thrombotic occlusion of right coronary artery (RCA) and unsuccessful primary percutaneous coronary intervention (PCI) complicated by refractory RVF managed with an Impella RP device.A total of 5 patients have been treated. The mean age was 73 ± 9 years, 80% were males. All patients, except one, were hemodynamically stable at hospital admission. In all patients, PCI resulted unsuccessful (final TIMI flow 3), with subsequent development of refractory RVF and cardiogenic shock in the catheterization laboratory, despite the use of inotropes and intra-aortic balloon pump (IABP). In 80% of the cases, Impella RP was placed immediately after PCI. Hemodynamics improved immediately after initiation of Impella RP support, with an increase in systolic blood pressure from 91 ± 17 to 136 ± 13 mmHg, a decrease in central venous pressure from 16 ± 2.5 to 12 ± 4 mmHg and a resolution in lactates from 4.5 ± 2.5 to 1.6 ± 0.7 mg/dL. Mean duration of IABP and Impella RP support were 4 and 7 days, respectively. RV recovery occurred in 80% of the cases. All patients survived at 30-day.In patients with AMI complicated by unsuccessful revascularization of RCA and refractory RVF, the use of Impella RP device resulted in immediate hemodynamic benefit with reversal of shock and favourable survival at 30-day.

Heart rate plays a major role in myocardial ischemia. A high heart rate increases myocardial performance and oxygen demand and reduces diastolic time. Ivabradine reduces heart rate by inhibiting the If current of sinoatrial-node cells. In contrast to beta-blockers, ivabradine has no negative inotropic and lusitropic effect for a comparable heart rate reduction. Consequently, diastolic duration is increased with ivabradine compared to beta-blockers. This has potential consequences on coronary blood flow since compression of the vasculature by the surrounding myocardium during systole impedes flow and coronary blood flow is mainly diastolic. Moreover, ivabradine does not unmask alpha-adrenergic vasoconstriction and, unlike beta-blockers, maintains coronary dilation during exercise. In comparison with beta-blockers, ivabradine increases coronary flow reserve and collateral perfusion promoting the development of coronary collaterals. Ivabradine attenuates myocardial ischemia and its consequences even in the absence of heart rate reduction, possibly through reduced formation of reactive oxygen species. In conclusion, ivabradine differs from other anti-anginal agents by improving coronary blood flow and by additional pleiotropic effects. These properties make ivabradine an effective anti-anginal and anti-ischemic agent for the treatment of patients with coronary artery disease.

Possible ethnic differences in clinical characteristics and long-term prognosis of contemporary patients with vasospastic angina (VSA) remain to be elucidated.The Japanese Coronary Spasm Association (JCSA) conducted an international, prospective, and multicenter registry study for VSA patients. A total of 1457 VSA patients (Japanese/Caucasians, 1339/118) were enrolled based on the same diagnostic criteria. Compared with Caucasian patients, Japanese patients were characterized by higher proportions of males (68 vs. 51%) and smoking history (60 vs. 49%). Japanese patients more often had angina especially during the night and early morning hours, compared with Caucasians. Ninety-five percent of Japanese and 84% of Caucasian patients underwent pharmacological provocation test. Importantly, no significant differences in the patterns of coronary spasm were apparent, with diffuse spasm most frequently noted in both ethnicities. The prescription rate of calcium-channel blockers was higher in Japanese (96 vs. 86%), whereas the uses of nitrates (46 vs. 59%), statins (43 vs. 65%), renin-angiotensin-system inhibitors (27 vs. 51%), and β-blockers (10 vs. 24%) were more common in Caucasian patients. Survival rate free from major adverse cardiac events (MACE) was slightly but significantly higher in Japanese than in Caucasians (86.7 vs. 76.6% at 5 years, P 0.001). Notably, multivariable analysis revealed that the JCSA risk score correlated with MACE rates not only in Japanese but also in Caucasian patients.These results indicate that there are ethnic differences in clinical profiles and long-term prognosis of contemporary VSA patients.

The European Union defines a rare disease as a condition that affects less than 5 in 10,000 of the general population. By this definition, there are between 6000 and 8000 known rare disorders that together affect 1 in 17 Europeans. For this reason, rare disorders are the subject of intense scrutiny by governments and healthcare organisations that are developing new systems for clinical care, research and patient involvement.

Coronary artery diseases and particularly acute myocardial infarction are the leading causes of mortality and morbidity in western countries. Despite the achievements of the last decades with the advent of double antiplatelet therapy, new antithrombotics and reperfusion strategies (either pharmacological or mechanical), many patients still have adverse cardiovascular events after ST-segment elevation acute myocardial infarction; at least some of these adverse events are related to the no reflow phenomenon that occurs after primary percutaneous coronary intervention. In our review we will discuss the various aspects of this phenomenon.

Background: Aim of the study was to investigate whether late gadolinium enhancement (LGE) at cardiac magnetic resonance (CMR) predict reverse remodeling (RR) in non-ischemic dilated cardiomyopathy (NIDCM). Methods: Seventy-one NIDCM patients (age 57. ±. 14. years, 43 males, median left ventricular ejection fraction [LVEF] 35%, [interquartile range 27-41%]) with two CMR scans within 5. years were included. RR was defined as ≥. 10% reduction in left ventricular (LV) end-diastolic volume and ≥. 10% LVEF increase. The end-point was a composite of all-cause death, cardiovascular hospitalization or appropriate defibrillator discharge. LGE was assessed both visually and as percentage of LV mass (LGE%). Results: LGE was present in 42 patients (59%). During the interval between the 2 CMR scans (median 28 [15-44]. months), 22 patients (31%) displayed RR. LGE absence predicted RR irrespectively of baseline LV volumes and LVEF. Over a median 42[15-73]-month follow-up, the endpoint occurred in 36 patients (51%). LGE absence was associated with better prognosis (P = 0.043), with best quantitative LGE cut-point

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In chronic heart failure (CHF) skeletal muscle insulin resistance occurs independently of etiology and contributes to impaired energy metabolism. GLUT4, the predominant glucose transporter in the skeletal muscle promotes the rate-limiting step of glucose utilization in skeletal muscle. The significance of skeletal muscle GLUT4 in patients with CHF has not been studied in detail.In patients with CHF and free of diabetes mellitus (n=29; mean NYHA class 2.3+/-0.1, peak VO(2) 18.8+/-1.1 mL/kg/min) and healthy control subjects of similar age (n=7), GLUT4 protein was assessed from percutaneous skeletal muscle biopsies. Skeletal muscle insulin sensitivity was assessed by intravenous glucose tolerance testing using a minimal modeling technique. Body composition was analyzed by dual energy X-ray absorptiometry (DEXA) scanning.Skeletal muscle GLUT4 was lower in CHF patients than in controls (0.75+/-0.07 vs 1.24+/-0.19 density units, P0.01) and decreased in parallel to severity of CHF, being lowest in NYHA III/IV (0.596+/-0.08, ANOVA P0.01 vs controls). GLUT4 was lower in patients with an ischemic etiology compared to dilated cardiomyopathy and controls (ANOVA P0.01). Patients and controls were similar for global parameters of body composition (weight: 78+/-4 vs 76+/-4 kg, BMI 25.5+/-0.8 vs 25.8+/-1.5 kg/m(2)), and total tissue amount and regional distribution of fat and lean tissue (all P0.2). Low GLUT4 predicted impaired insulin sensitivity, i.e. insulin resistance (r=0.55, P0.01). In multivariate analysis, GLUT4 levels predicted insulin sensitivity independently of age and parameters of body composition (including weight, BMI, and total and regional fat and lean tissue distribution).In non-diabetic patients with CHF, skeletal muscle GLUT4 transport protein is reduced in parallel to disease severity, independently of body composition. Low skeletal muscle GLUT4 contributes to insulin resistance in CHF.

multinational survey to evaluate the proportion of patients achieving low-density lipoprotein cholesterol goals. Circulation 2009;120:28–34. [9] Olsson AG, Lindahl C, Holme I, et al. LDL cholesterol goals and cardiovascular risk during statin treatment: the IDEAL study. Eur J Cardiovasc Prev Rehabil 2011;18:262–9. [10] Melloni C, Shah BR, Ou FS, et al. Lipid-lowering intensification and low-density lipoprotein cholesterol achievement from hospital admission to 1-year follow-up after an acute coronary syndrome event: results from theMedications ApplIed aNd SusTAINed Over Time (MAINTAIN) registry. Am Heart J 2010;160:1121–9.

Myocardial infarction in persons aged below 45 years is a rareevent, usually not related to coronary atherosclerosis, but mostly oc-curs as a consequence of cocaine abuse, congenital coronary abnor-malities, or spasm. We present the case of a young man with anacute anterior myocardial infarction caused by a rare protein defi-ciency in the coagulation system.A29‐year-oldman,of Africandescent,withnopriorhistoryof car-diac event, presented at our emergency department complaining ofsevere acute chest pain radiating to the left arm. Electrocardiographyshowed 2 mm ST elevation in V1 to V4. Transthoracic echocardiogra-phy revealed akinesia of the anterior wall and apex with mild globaldysfunction (ejection fraction 50%). Loading doses of ASA andclopidogrel were administered before coronary angiography thatshowed a large proximal thrombus in the left anterior descending cor-onary artery (LAD) causing total occlusion. Intracoronary abciximabwas administered, and, given large clot burden, thrombus aspirationwas performed before deploying two bare metal stents. At the endof the procedure the patient developed cardiogenic shock requiringadrenaline administration and IABP. Despite arterial patency beingrestored, TIMI flow 1 persisted in the LAD (Fig. 1A).Afterwards,contrast-enhancedcardiacmagneticresonance(CMR)showed transmural infarct of left ventricular apex that appeared thinand akinetic and multiple necrosis foci on interventricular septum(Fig. 1B). A complete thrombophilic screening was carried out, finallyrevealing a combined deficiency of proteins S and C: plasma protein Cand S concentration were respectively 39% and 43% of normal. A ther-apy with low molecular weight heparin was started at a dosage of6000 IU once daily, and 12 months dual antiplatelet therapy was rec-ommended. Two months later therapy was converted to oral antico-agulant with dabigatran 220 mg once daily. At 6 months follow up,the patient remained asymptomatic. Family history revealed recur-rence of severe thromboembolism among his relatives.Protein C is a vitamin K-dependentprotein, synthesized in theliver,that inactivates coagulation factors Va and VIIIa, which are required tothrombin generation and factor X activation. This process is stronglysupported by protein S activity as cofactor. Moreover Protein C hasestablished antin flammatory activity and seems to harbor cyto-protectivepropertiesonendothelialcells.Itisestimatedthatcongenitalprotein C deficiency is present in 2 to 5% of patients with thromboem-bolism [1]. Prevalence of clinically symptomatic deficiencies of proteinC in the general population lies between 1:16,000 and 1:36,000 whilethat of symptomatic protein S deficiency is 1:20,000. Both protein Cand S deficiencies are associated with increased risk of developingdeep venous thrombosis (risk ratio 8.1 for protein S deficiency and 7.3for protein C deficiency) [2] and higher risk of recurrent thrombosis,with typically young age of onset and family cluster occurrence. Thefew available reports of families with combined protein C and S defi-ciency suggest that both genes segregate independently as an autoso-mal dominant trait. Although venous district is typically involved(deep veins, pulmonary artery, jugular vein), arterial thrombosis hasbeen reported. Aorta, mesenteric and cerebral arteries can be affected[3]. Patients with C protein deficiency are at potential risk of warfarininduced skin necrosis, and for that we preferred LMWE and dabigatranto vitamin K antagonist.After acute myocardial infarction inadequate tissue perfusion mayoccur despite early and successful reopening of the infarct-related ar-tery with primary percutaneous coronary intervention. This situation,known as “No Reflow” (NR), significantly affects outcome [4]. NR canbe related to ischemia-reperfusion injury or to downstream emboli-zation of atherosclerotic material into the microvasculature. CMR al-lows the detection of myocardial injury with high accuracy: theintensity of myocardial enhancement is related to expansion of theinterstitial volume secondary to cell necrosis; persistent hypo-perfusion on first pass contrast-enhanced images suggests microvas-cular obstruction (Fig. 2A), which impedes delivery of contrastmedium, or dysfunction of coronary microvasculature that can be re-liably assessed by positron emission tomography (Fig. 2B).Current approaches for prevention and treatment of NR includevasodilators, glycoprotein IIb/IIIa inhibitors and thrombus aspiration.Although we used all of the above, the patient did not achievesuccessful reperfusion. Thrombophilia may have contributed to ex-tensive myocardial damage through a greater and diffuse pro