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An increase in left atrial (LA) size in patients with arterial hypertension (AHT) has long been known to be associated with worse cardiovascular morbidity and mortality contributes to various complications, including atrial arrhythmias, stroke, and heart failure. The aim of our study was to evaluate the impact of arterial hypertension (AHT) on the LA size and function. This cross-sectional investigation included one hundred patients with essential hypertension without valvular or structural heart disease and atrial fibrillation. All recruits had a transthoracic echocardiography. LA volumes were measured by area-length method in transthoracic echocardiography at different cardiac cycle times. The indices of LA function were calculated: the reservoir function (total emptying fraction, total emptying volume, and expansion index), the conduit function (passive emptying fraction and passive emptying volume), and the pump function (active emptying fraction and active emptying volume). For all statistical tests, a p value ≤0.05 (represents the degree of significance) is considered statistically significant. In univariate analysis, LA was dilated in 9% of patients. The LA reservoir function and the pump function were increased, respectively, in 85% and 82% of patients. LA conduit function was impaired in 80% of patients. In bivariate analysis, the most powerful factors for this repercussion were diabetes (LA volume MAX dilated in nondiabetic patients (p = 0.037)), obesity (the reservoir function was impaired in obese patients (p = 0.015)), and antihypertensive drugs (the reservoir function was impaired in patients who take beta blockers (p = 0.023); the LA pump function was significantly impaired in patients treated with calcium antagonists (p = 0.012)). This study proved the impact of AHT on the LA size and function. Further investigations are necessary to evaluate the potential predictive value of LA remodeling in hypertensive patients like speckle tracking imaging. [ABSTRACT FROM AUTHOR]

An increase in left atrial (LA) size in patients with arterial hypertension (AHT) has long been known to be associated with worse cardiovascular morbidity and mortality contributes to various complications, including atrial arrhythmias, stroke, and heart failure. The aim of our study was to evaluate the impact of arterial hypertension (AHT) on the LA size and function. This cross-sectional investigation included one hundred patients with essential hypertension without valvular or structural heart disease and atrial fibrillation. All recruits had a transthoracic echocardiography. LA volumes were measured by area-length method in transthoracic echocardiography at different cardiac cycle times. The indices of LA function were calculated: the reservoir function (total emptying fraction, total emptying volume, and expansion index), the conduit function (passive emptying fraction and passive emptying volume), and the pump function (active emptying fraction and active emptying volume). For all statistical tests, a p value ≤0.05 (represents the degree of significance) is considered statistically significant. In univariate analysis, LA was dilated in 9% of patients. The LA reservoir function and the pump function were increased, respectively, in 85% and 82% of patients. LA conduit function was impaired in 80% of patients. In bivariate analysis, the most powerful factors for this repercussion were diabetes (LA volume MAX dilated in nondiabetic patients (p = 0.037)), obesity (the reservoir function was impaired in obese patients (p = 0.015)), and antihypertensive drugs (the reservoir function was impaired in patients who take beta blockers (p = 0.023); the LA pump function was significantly impaired in patients treated with calcium antagonists (p = 0.012)). This study proved the impact of AHT on the LA size and function. Further investigations are necessary to evaluate the potential predictive value of LA remodeling in hypertensive patients like speckle tracking imaging. [ABSTRACT FROM AUTHOR]

Persistent cardiovascular pathology has been described in hyperthyroid patients even with effective antithyroid treatment. Here, we studied the effect of a well-known antithyroid drug, propylthiouracil (PTU; 20 mg/kg/day), on thyroxine (T4; 500 µg/kg/day)-induced increase in blood pressure (BP), cardiac hypertrophy, and altered responses of the contractile myocardium both in vivo and ex vivo after 2 weeks of treatment. Furthermore, the potential recovery through 2 weeks of T4 treatment discontinuation was also investigated. PTU and T4 recovery partially reduced the T4-prompted increase in BP. Alternatively, PTU significantly improved the in vivo left ventricular (LV) function with no considerable effects on cardiac hypertrophy or ex vivo right ventricular (RV) contractile alterations subsequent to T4 treatment. Conversely, T4 recovery considerably enhanced the T4-provoked cardiac changes both in vivo and ex vivo. Altogether, our data is in agreement with the proposal that hyperthyroidism-induced cardiovascular pathology could persevere even with antithyroid treatments, such as PTU. However, this cannot be generalized and further investigation with different antithyroid treatments should be executed. Moreover, we reveal that recovery following experimental hyperthyroidism could potentially ameliorate cardiac function and decrease the risk for additional cardiac complications, yet, this appears to be model-dependent and should be cautiously construed. [ABSTRACT FROM AUTHOR]

The relationship and clinical implications of atrial fibrillation (AF) in acute pulmonary embolism (PE) are poorly investigated. We aimed to analyze clinical characteristics and prognosis in PE patients with paroxysmal AF episode. Methods. From the 391 patients with PE 31 subjects with paroxysmal AF were selected. This group was compared with patients with PE and sinus rhythm (SR) and 32 patients with PE and permanent AF. Results. Paroxysmal AF patients were the oldest. Concomitant DVT varies between groups: paroxysmal AF 32.3%, SR 49.5%, and permanent AF 28.1% (p=0.02). The stroke history frequency was 4.6% SR, 12.9% paroxysmal AF, and 21.9% permanent AF (p<0.001). Paroxysmal AF comparing to permanent AF and SR individuals had higher estimated SPAP (56 versus 48 versus 47 mmHg, p=0.01) and shorter ACT (58 versus 65 versus 70 ms, p=0.04). Patients with AF were more often classified into high-risk group according to revised Geneva score and sPESI than SR patients. In-hospital mortality was lower in SR (5%) and paroxysmal AF (6.5%) compared to permanent AF group (25%) (p<0.001). Conclusions. Patients with PE-associated paroxysmal AF constitute a separate population. More severe impairment of the parameters reflecting RV afterload may indicate relation between PE severity and paroxysmal AF episode. Paroxysmal AF has no impact on short-term mortality. [ABSTRACT FROM AUTHOR]

Background. The aim of this study is to show whether the septal E/(E′×S′) ratio assessed by tissue Doppler echocardiography can predict left ventricular remodeling after first ST segment elevation myocardial infarction treated successfully with primary percutaneous intervention. Methods. Consecutive patients (n=111) presenting with acute anterior myocardial infarction for the first time in their life were enrolled. All patients underwent successful primary percutaneous coronary intervention. Standard and tissue Doppler echocardiography were performed in the first 24-36 hours of admission. Echocardiographic examination was repeated after 6 months to reassess left ventricular volumes. Septal E/(E′×S′) ratio was assessed by pulsed Doppler echocardiography. Results. Group 1 consisted of 33 patients with left ventricular (LV) remodeling, and Group 2 had 78 patients without LV remodeling. E/(E′×S′) was significantly higher in Group 1 (4.1±1.9 versus 1.65±1.32, p=0.001). The optimal cutoff value for E/(E′×S′) ratio was 2.34 with 87.0% sensitivity and 82.1% specificity. Conclusion. Septal E/(E′×S′) values measured after the acute anterior myocardial infarction can strongly predict LV remodeling in the 6-month follow-up. In the risk assessment, the septal E/(E′×S′) can be evaluated together with the conventional echocardiographic techniques. [ABSTRACT FROM AUTHOR]

Objectives. We investigated whether amlodipine could improve angiogenic responses in a diabetic rat model of acute myocardial infarction (AMI) through improving bone marrow endothelial progenitor cell (EPC) mobilization, in the same way as angiotensin converting enzyme inhibitors. Methods. After induction of AMI by coronary artery ligation, diabetic rats were randomly assigned to receive perindopril (2 mgkg−1 day−1), amlodipine (2.5 mgkg−1 day−1), or vehicle by gavage (n=20 per group). Circulating EPC counts before ligation and on days 1, 3, 5, 7, 14, and 28 after AMI were measured in each group. Microvessel density, cardiac function, and cardiac remodeling were assessed 4 weeks after treatment. The signaling pathway related to EPC mobilization was also measured. Results. Circulating EPC count in amlodipine- and perindopril-treated rats peaked at day 7, to an obvious higher level than the control group peak which was reached earlier (at day 5). Rats treated with amlodipine showed improved postischemia neovascularization and cardiac function, together with reduced cardiac remodeling, decreased interstitial fibrosis, and cardiomyocyte apoptosis. Amlodipine treatment also increased cardiac SDF-1/CXCR4 expression and gave rise to activation of VEGF/Akt/eNOS signaling in bone marrow. Conclusions. Amlodipine promotes neovascularization by improving EPC mobilization from bone marrow in diabetic rats after AMI, and activation of VEGF/Akt/eNOS signaling may in part contribute to this. [ABSTRACT FROM AUTHOR]

Background. Analyses emphasizing gender-related differences in acute and long-term outcomes following MitraClip therapy for significant mitral regurgitation (MR) are rare. Methods. 592 consecutive patients (75±8.7 years, 362 men, 230 women) underwent clinical and echocardiographic follow-up for a median of 2.13 (0.99–4.02) years. Results. Significantly higher prevalence of cardiovascular comorbidities, renal failure, and adverse echocardiographic parameters in men resulted in longer device time (p=0.007) and higher numbers of implanted clips (p=0.0075), with equal procedural success (p=1.0). Rehospitalization for heart failure did not differ (p[logrank]=0.288) while survival was higher in women (p[logrank]=0.0317). Logarithmic increase of NT-proBNP was a common independent predictor of death. Hypercholesterolemia and peripheral artery disease were predictors of death only in men while ischemic and dilative cardiomyopathy (CM) and age were predictors in women. Independent predictors of rehospitalization for heart failure were severely reduced ejection fraction and success in men while both ischemic and dilative CM, logistic EuroSCORE, and MR severity were predictive in women. Conclusions. Higher numbers of implanted clips and longer device time are likely related to more comorbidities in men. Procedural success and acute and mid-term clinical outcomes were equal. Superior survival for women in long-term analysis is presumably attributable to a comparatively better preprocedural health. [ABSTRACT FROM AUTHOR]

Left ventricular end-diastolic pressure (LVEDP) is the foundation of cardiac function assessment. Because of difficulties and risks associated with its direct measurement, correlates of LVEDP derived by pulmonary artery (PA) catheterization or transesophageal echocardiography (TEE) are commonly adopted. TEE has the advantage of being less invasive; however TEE-based estimation of LVEDP using correlates such as left ventricular end-diastolic volume (LVEDV) has technical difficulties that limit its clinical usefulness. Using intraoperative acute normovolemic hemodilution (ANH) as a controlled hemorrhagic model, we examined various mitral flow parameters and three-dimensional reconstructions of left atrial volume as surrogates of LVEDP. Our results demonstrate that peak E wave velocity and left atrial end-diastolic volume (LAEDV) correlated with known changes in intravascular volume associated with ANH. Although left atrial volumetric analysis was done offline in our study, recent advances in echocardiographic software may allow for continuous display and real-time calculation of LAEDV. Along with the ease and reproducibility of acquiring Doppler images of flow across the mitral valve, these two correlates of LVEDP may justify a more widespread use of TEE to optimize intraoperative fluid management. The clinical applicability of peak E wave velocity and LAEDV still needs to be validated during uncontrolled resuscitation. [ABSTRACT FROM AUTHOR]

Background. Maze procedure aims at restoring sinus rhythm (SR) and atrial contractility (AC). This study evaluated multiple aspects of AC recovery and their relationship with SR regain after ablation. Methods. 122 mitral and fibrillating patients underwent radiofrequency Maze. Rhythm check and echocardiographic control of biatrial contractility were performed at 3, 6, 12, and 24 months postoperatively. A multivariate Cox analysis of risk factors for absence of AC recuperation was applied. Results. At 2-years follow-up, SR was achieved in 79% of patients. SR-AC coexistence increased from 76% until 98%, while biatrial contraction detection augmented from 84 to 98% at late stage. Shorter preoperative arrhythmia duration was the only common predictor of SR-AC restoring, while pulmonary artery pressure (PAP) negatively influenced AC recuperation. Early AC restoration favored future freedom from arrhythmia recurrence. Minor LA dimensions correlated with improved future A/E value and vice versa. Right atrial (RA) contractility restoring favored better left ventricular (LV) performance and volumes. Conclusions. SR and left AC are two interrelated Maze objectives. Factors associated with arrhythmia “chronic state” (PAP and arrhythmia duration) are negative predictors of procedural success. Our results suggest an association between postoperative LA dimensions and “kick” restoring and an influence of RA contraction onto LV function. [ABSTRACT FROM AUTHOR]

Oncostatin M (OSM) has been reported to stimulate angiogenesis by upregulating VEGF and bFGF, implying that it could be a therapeutic strategy in treating ischemic diseases. The present study was aimed at investigating whether OSM could improve cardiac function via prompting angiogenesis following myocardial infarction (MI). Wild type (WT) and Oβ knock-out (Oβ−/−) mice were, respectively, randomized into sham group, MI + vehicle group, and MI + OSM group. WT mice displayed significantly impaired cardiac function after MI. OSM treatment attenuated cardiac dysfunction in WT MI mice, while Oβ deletion abrogated the protective effects. Besides, OSM attenuated heart hypertrophy and pulmonary congestion evidenced by decreased heart weight/body weight and lung weight/body weight ratio. Further, reduction of apoptosis and fibrosis in infarct border zone was observed in OSM treated WT MI mice compared with vehicle. Moreover, in WT mice subjected to MI, OSM treatment significantly increased capillary density along with upregulation of p-Akt and angiogenic factors VEGF and bFGF in comparison with vehicle, and this phenomenon was not found in Oβ−/− mice. In conclusion, OSM treatment preserved cardiac function, inhibited apoptosis and fibrosis, and stimulated angiogenesis via upregulating VEGF and bFGF in infarct border zone of ischemic myocardium, indicating that OSM could be a novel therapeutic target for MI. [ABSTRACT FROM AUTHOR]