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Concept: Left ventricular hypertrophy


The classic Morrow technique for hypertrophic obstructive cardiomyopathy (HOCM) in patients with simultaneous obstruction of left ventricular (LV) midcavity and right ventricular outflow tract (RVOT) combined with extreme left ventricular hypertrophy, is not effective. A new technique for HOCM surgical correction in patients with severe hypertrophy is proposed.

Concepts: Cardiology, Cardiomyopathy, Left-wing politics, Left ventricular hypertrophy, Hypertrophic cardiomyopathy, Political spectrum, Hypertrophy


: We determined whether left ventricular hypertrophy (LVH) which exceeds that predicted from workload [inappropriate LV mass (LVMinappr)] is associated with reduced left ventricle (LV) systolic chamber function independent of and more closely than absolute or indexed left ventricular mass (LVM).

Concepts: Cardiology, Left ventricular hypertrophy, Right ventricle, Ventricle, Ventricular hypertrophy, Left ventricle


BackgroundTo determine the prognostic value of various self-blood pressure (BP) monitoring (SBPM) cutoff at the time of diagnosis.MethodsCohort of 466 newly diagnosed and never-treated hypertensive patients. At baseline and at 1 year, the patients underwent a physical examination, clinic BP (CBP), SBPM, and ambulatory BP monitoring (ABPM), fasting blood and urine analysis, electrocardiogram (ECG), and retinography. The diagnosis of hypertension was made based on CBP average of two readings, separated by 2 min, taken over three different days, with results ≥140/90 mm Hg. At 1-year follow-up, target organ damage (TOD) evolution was classified as favorable or unfavorable.ResultsMean age was 57.4 years, 56.8% were men. Adjusted multivariate analysis showed that hypertensive patients with baseline SBPM <135/85 mm Hg had a more favorable evolution of left ventricular hypertrophy (LVH) (odds ratio (OR): 1.9; 95% confidence interval (CI): 1.5-2.5), high urinary albumin excretion rate (UAER) (OR: 6.9; 95% CI: 3.4-14.4), and more favorable amount of TOD evolution (OR: 1.7; 95% CI: 1.4-2.0) than those with baseline SBPM ≥135/85 mm Hg. Patients with baseline SBPM <130/80 mm Hg, or <125/80 mm Hg had a more favorable evolution of the amount of TOD (OR: 2.7; 95% CI: 2.0-3.6, and OR: 2.9; 95% CI: 2.1-4.1, respectively) at 1 year than those with baseline SBPM <135/85 mm Hg.ConclusionsBaseline SBPM values <130/80 mm Hg is associated with better evolution of amount of TOD than SBPM values <135/85 mm Hg. These results would support a clinical trial to test a SBPM threshold <130/80 as an optimal pressure not needing pharmacological treatment among those with CBP ≥140/90.American Journal of Hypertension 2012; doi:10.1038/ajh.2012.126.

Concepts: Nephrology, Hypertension, Urine, Cardiology, Left ventricular hypertrophy, Retina, Ventricular hypertrophy, End organ damage


Angiotensin-converting enzyme inhibitors (ACEIs) are the first-line therapy for the treatment of hypertension. However, not all ACEIs are equal. Delapril is a nonsulfhydryl ACEI with unique properties. Delapril has a high lipophilicity and weak bradykinin potentiating action. As a result, delapril has a more potent inhibition capacity of vascular wall angiotensin-converting enzyme activity and a lower incidence of cough than enalapril or captopril. With regard to efficacy, delapril has a long-lasting antihypertensive effect with a trough/peak ratio that is in the upper range of different ACEIs and a positively high smoothness index. Thus, delapril effectively and smoothly reduces blood pressure over 24 h. Moreover, the benefits of delapril are not limited to hypertensive patients, but also in those with microalbuminuria, left ventricular hypertrophy, myocardial infarction or heart failure; delapril appears to be effective and well tolerated.

Concepts: Myocardial infarction, Hypertension, Cardiology, Heart failure, Blood pressure, Left ventricular hypertrophy, ACE inhibitor, Captopril


Left ventricular hypertrophy (LVH) regression is an important issue in hypertensive patients. Patients with LVH who had received the angiotensin receptor blocker (ARB) treatment for 8 weeks and had not reached the target blood pressure level were enrolled in the study. Patients were assigned to either losartan (50 mg)/hydrochlorothiazide (HCTZ, 12.5 mg) group or ARB + CCB group (usual dose of ARB and calcium channel blocker, CCB). After 48 weeks, LV mass index was found to be reduced significantly in the losartan/HCTZ group but not in the ARB + CCB group. These results suggest that combination therapy of an ARB and diuretic has greater potential to cause regression compared with an ARB and CCB.

Concepts: Hypertension, Cardiology, Blood pressure, Left ventricular hypertrophy, Angiotensin, Renin-angiotensin system, Angiotensin II receptor antagonist, Angiotensin receptor


BACKGROUND: Most sudden deaths during sports occur in general population practising recreational sports and according to legislation, a forensic autopsy is required. Most are sudden cardiac deaths but the incidence of specific pathologies differs in reported series according to autopsy methods or diagnostic criteria. The purpose of this work is to analyse the pathology of sports-related sudden deaths in a large forensic series from Spain studied according with cardiovascular pathology criteria. MATERIALS AND RESULTS: We have reviewed the sudden deaths occurred during sports studied at our institution between 1995 and 2010 in which a complete autopsy was performed with exhaustive cardiac examination and toxicological analysis. Out of 8862 sudden deaths studied, 168 (1.8%) were related to sports; age was between 9 and 69 (average 36.6±15.6y); 163 were males and 5 females. Only 3 were professional athletes. Most frequent sports associated to sudden death were cycling (29%), soccer (25.5%), running (8.9%) and gymnastics (6.5%). In 49 cases (29.1%) there were some personal pathological antecedents or familial sudden deaths. Causes of death were: coronary atherosclerotic disease, 85 (50.5%) (74 over 35 years old); arrhythmogenic cardiomyopathy, 13 (7.7%); hypertrophic cardiomyopathy, 12 (7.1%); idiopathic left ventricular hypertrophy, 7 (4.1%); congenital coronary anomalies, 7 (4.1%); myocarditis, 6 (3.5%); aortic stenosis, 5 (2.9%); and other, 11 (6.5%). Myocardial diseases were the most frequent under 35 years old. No cause of death was found in 19 (11.3%) (all under 30 years old) what stresses the necessity of including molecular techniques in forensic autopsies.

Concepts: Death, Atherosclerosis, Pathology, Cardiology, Heart, Left ventricular hypertrophy, Hypertrophic cardiomyopathy, Autopsy


-Left ventricular (LV) hypertrophy (LVH, high LV mass) is traditionally classified as concentric or eccentric based on LV relative wall thickness. We evaluated the prediction of subsequent adverse events in a new 4-group LVH classification based on LV dilatation (high LV end-diastolic volume [EDV] index) and concentricity (LVM/EDV((2/3))) in hypertensive patients.

Concepts: Hypertension, Cardiology, Left ventricular hypertrophy, Geometry, Ventricular hypertrophy, Aortic insufficiency, Cardiomegaly


Current electrocardiographic (ECG) criteria for the diagnosis of left ventricular hypertrophy (LVH) have low sensitivity.

Concepts: Cardiology, Left ventricular hypertrophy


Background Fabry’s disease, an X-linked disorder of lysosomal α-galactosidase deficiency, leads to substrate accumulation in multiple organs. Migalastat, an oral pharmacologic chaperone, stabilizes specific mutant forms of α-galactosidase, increasing enzyme trafficking to lysosomes. Methods The initial assay of mutant α-galactosidase forms that we used to categorize 67 patients with Fabry’s disease for randomization to 6 months of double-blind migalastat or placebo (stage 1), followed by open-label migalastat from 6 to 12 months (stage 2) plus an additional year, had certain limitations. Before unblinding, a new, validated assay showed that 50 of the 67 participants had mutant α-galactosidase forms suitable for targeting by migalastat. The primary end point was the percentage of patients who had a response (≥50% reduction in the number of globotriaosylceramide inclusions per kidney interstitial capillary) at 6 months. We assessed safety along with disease substrates and renal, cardiovascular, and patient-reported outcomes. Results The primary end-point analysis, involving patients with mutant α-galactosidase forms that were suitable or not suitable for migalastat therapy, did not show a significant treatment effect: 13 of 32 patients (41%) who received migalastat and 9 of 32 patients (28%) who received placebo had a response at 6 months (P=0.30). Among patients with suitable mutant α-galactosidase who received migalastat for up to 24 months, the annualized changes from baseline in the estimated glomerular filtration rate (GFR) and measured GFR were -0.30±0.66 and -1.51±1.33 ml per minute per 1.73 m(2) of body-surface area, respectively. The left-ventricular-mass index decreased significantly from baseline (-7.7 g per square meter; 95% confidence interval [CI], -15.4 to -0.01), particularly when left ventricular hypertrophy was present (-18.6 g per square meter; 95% CI, -38.2 to 1.0). The severity of diarrhea, reflux, and indigestion decreased. Conclusions Among all randomly assigned patients (with mutant α-galactosidase forms that were suitable or not suitable for migalastat therapy), the percentage of patients who had a response at 6 months did not differ significantly between the migalastat group and the placebo group. (Funded by Amicus Therapeutics; numbers, NCT00925301 [study AT1001-011] and NCT01458119 [study AT1001-041].).

Concepts: Renal failure, Kidney, Enzyme, Medical terms, Glomerulus, Left ventricular hypertrophy, Renal physiology, Renal function


The electrocardiogram (ECG) is the most commonly used tool to screen for left ventricular hypertrophy (LVH), and yet current diagnostic criteria are insensitive in modern increasingly overweight society. We propose a simple adjustment to improve diagnostic accuracy in different body weights and improve the sensitivity of this universally available technique.

Concepts: Diagnosis, Cardiology, Left ventricular hypertrophy, Ventricular hypertrophy, Ventricular fibrillation