Concept: Ventricular 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).
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.
-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.
In response to pressure overload, the heart develops ventricular hypertrophy that progressively decompensates and leads to heart failure. This pathological hypertrophy is mediated, among others, by the phosphatase calcineurin and is characterized by metabolic changes that impair energy production by mitochondria.
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.
Growth differentiation factor 11 and/or its homologue growth differentiation factor 8 (GDF11/8) reverses age-related cardiac hypertrophy and vascular ageing in mice. We investigated whether GDF11/8 associates with cardiovascular outcomes, left ventricular hypertrophy (LVH), or age in humans.
Left ventricular hypertrophy (LVH) and myocardial contractile dysfunction are independent predictors of mortality in patients with chronic kidney disease (CKD). The association between inflammatory biomarkers and cardiac geometry has not yet been studied in a large cohort of CKD patients with a wide range of kidney function.
- Journal of applied physiology (Bethesda, Md. : 1985)
- Published over 2 years ago
Left ventricular hypertrophy (LVH) is the most common myocardial structural abnormality associated with heart failure with preserved ejection fraction (HFpEF). LVH is driven by neurohumoral activation, increased mechanical load and cytokines associated with arterial hypertension, chronic kidney disease, diabetes and other co-morbidities. Here we discuss the experimental and clinical evidence that links LVH to diastolic dysfunction and qualifies LVH as one diagnostic marker for HFpEF. Mechanisms leading to diastolic dysfunction in LVH are incompletely understood but may include extracellular matrix changes, vascular dysfunction as well as altered cardiomyocyte mechano-elastical properties. Beating cardiomyocytes from HFpEF patients have not yet been studied, but we and others have shown increased Ca(2+) turnover and impaired relaxation in cardiomyocytes from hypertrophied hearts. Structural myocardial remodeling can lead to heterogeneity in regional myocardial contractile function, which contributes to diastolic dysfunction in HFpEF. In the clinical setting of patients with compound co-morbidities, diastolic dysfunction may occur independently of LVH. This may be one explanation why current approaches to reduce LVH have not been effective to improve symptoms and prognosis in HFpEF. Exercise training on the other hand, in clinical trials improved exercise tolerance and diastolic function but did not reduce LVH. Thus, current clinical evidence does not support regression of LVH as a surrogate marker for (short-term) improvement of HFpEF.
Asymptomatic left ventricular hypertrophy (LVH) is highly prevalent and associated with an adverse outcome in renal transplant recipients (RTRs). Nonetheless, there are currently no available studies analyzing the effect of LVH regression on solid clinical endpoints in these patients.
The purpose of this study was to determine among maintenance hemodialysis patients with echocardiographic left ventricular hypertrophy and hypertension whether in comparison with a β-blocker-based antihypertensive therapy, an angiotensin converting enzyme-inhibitor-based antihypertensive therapy causes a greater regression of left ventricular hypertrophy.