Evolution Of Left Ventricular Hypertrophy Research Articles

Autophagy Portends the Level of Cardiac Hypertrophy in Experimental Hypertensive Swine Model.

Left ventricular (LV) hypertrophy (LVH) plays an important role in hypertensive heart disease, and may be accompanied by myocardial autophagy. However, the pattern of autophagy during evolution of LVH is unclear. We hypothesized that autophagy activation indicates advancing cardiac LVH with tissue remodeling. Ten domestic pigs with a 10-week unilateral renovascular hypertension (HTN) were classified as mild or moderate HTN (n = 5 each group) based on the degree of renal artery stenosis (above or below 75%). Seven normal pigs served as controls. Left ventricular remodeling, function, and microvascular density were assessed using multi-detector- and micro-computed tomography and histology. Markers of myocardial autophagic and endoplasmic reticulum (ER) stress-related unfolded protein response (UPR), apoptosis, and fibrosis were examined ex vivo. Both HTN groups had increased myocyte cross-sectional area, but it was greater in moderate HTN, accompanied by elevated LV muscle-mass. Moderate, but not mild HTN, also showed impaired microvascular density and impaired myocardial perfusion. Autophagy mediators were unaltered in mild HTN but UPR markers were increased, while in moderate HTN they were all upregulated, whereas UPR markers were suppressed. Myocardial apoptosis and fibrosis were also greater in moderate HTN. Autophagic proteins were correlated with LVH and fibrosis. Autophagic activity is stimulated during the exacerbation of LVH, following a transient early increase in ER stress, and may be involved in the progression of cardiac remodeling in renovascular hypertensive heart disease.

Retinal arteriole-to-venule ratio changes and target organ disease evolution in newly diagnosed hypertensive patients at 1-year follow-up

There is no agreement on the systematic exploration of the fundus oculi (FO) in hypertensive patients, and it is unknown whether the evolution of retinal microcirculatory alterations has prognostic value or not. The aim of this study was to investigate whether the evolution of the arteriole-to-venule ratio (AVR) in newly-diagnosed hypertensive patients is associated with better or worse evolution of target organ damage (TOD) during 1 year. A cohort of 133 patients with newly-diagnosed untreated hypertension was followed for 1 year. At baseline and follow-up, all patients underwent a physical examination, self-blood pressure measurement, ambulatory blood pressure monitoring, blood and urine analysis, electrocardiogram, and retinography. The endpoint was the favourable evolution of TOD and the total amount of TOD, according to the baseline AVR and the baseline and final difference of the AVR. A total of 133 patients were analyzed (mean age, 57 ± 10.7 years; 59% men). No differences were found in the decrease in blood pressure or antihypertensive treatment between quartiles of baseline AVR or baseline-final AVR difference. Patients with a difference between baseline and final AVR in the highest quartile (>0.0817) had a favorable evolution of left ventricular hypertrophy (odds ratio, 14.9; 95% confidence interval, 1.08–206.8) and the amount of TOD (odds ratio, 2.22; 95% confidence interval, 1.03–6.05). No favorable evolution was found of glomerular filtration rate. There is an association between the evolution of the AVR and the favorable evolution of TOD. Patients with greater increase of AVR have significantly better evolution of left ventricular hypertrophy and amount of TOD.

Evolution of Target Organ Damage by Different Values of Self-Blood Pressure Measurement in Untreated Hypertensive Patients

To determine the prognostic value of various self-blood pressure (BP) monitoring (SBPM) cutoff at the time of diagnosis. Cohort 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. Mean 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. Baseline 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.

Determinants of evolution of ECG signs of left ventricular hypertrophy during long-term antihypertensive treatment in patients with high risk arterial hypertension

Objective: to study the evolution of ECG left ventricular hypertrophy (LVH) in patients with high risk arterial hypertension (AH) with during long-term antihypertensive treatment. Design and methods. 102 patients (48% males, average age 67,1+0,6) with AH of high risk were randomized to antihypertensive therapy based on AT1 angiotensine II receptors anatagonists (ARA) or dihydropiridine calcium channel blockers (CCB). To achieve target blood pressure (BP) 35 mV, Cornell voltage criteria>20 mV in females and > 28 mV in males and Cornell product >2442 msec*mV). Results: In 1 year of treatment regress of LVH was observed in 8 from 31 (25,85%) patients with initially ECG- LVH. Patients with regress of ECG - LVH were younger and had lower BMI versus patients with of ECG-LVH persistence (65,5±2,4 vs 66,7±5,9 years and 28,6±5,6 vs 29,2±4,3 kg/m 2 respectively, n.s.); and significantly lower systolic BP (SBP) after 1 year treatment (137,8±7,6 mmHg vs 142,3±6,2 mmHg respectively). Step logistic regression analysis revealed that SBP was the only independent factor related with regress of ECG-LVH. baseline. Those patients were non significantly older (69,4±6,4 vs 66,0±6,2 years) and had higher blood glucose and total cholesterol levels both at baseline and after 1-year treatment and higher SBP after 1 treatment. Independent correlation with ECG-LVH development was found only for SBP, glucose and total cholesterol vlaues after 1-year treatment. There was no correlation between evolution of LVH and the type of treatmen. Conclusion. Persistence and development of ECG-LVH in patients with high risk AH during long-term antihypertensive treatment is mainly associated with insufficient SBP control. Data on value of glucose and total cholesterol levels suggests potential benefit of treatment regimens with complex correction of risk factors for prevention of ECG-LVH development.

Hypertrophy in the female heart

Several clinical studies have suggested that sex influences the left ventricle's response to altered loading conditions and thus the development of cardiac hypertrophy. Likewise, several of the risk factors associated with the development of hypertrophy exhibit sexual dimorphism in their distribution in the general population. These sex-specific differences in risk factor distribution are likely important modifiers in disease progression and outcome. This review explores the available evidence of sex-specific differences in the evolution of left ventricular hypertrophy.

Changes in left ventricular mass index in children and adolescents after renal transplantation.

Recent reports indicate a high prevalence of left ventricular hypertrophy (LVH) in children on dialysis and after renal transplantation (Tx), as identified by cross-sectional analysis. However, the evolution of LVH in pediatric patients with end-stage renal disease after renal Tx is not well established. To assess changes of left ventricular mass (LVM), we prospectively performed echocardiography in 23 children and adolescents between November 1998 and July 2000. Each patient had an echocardiographic evaluation while on dialysis (for at least 6 weeks) and a follow-up evaluation at least 6 months after successful renal Tx (i.e. with a measured glomerular filtration rate [GFR] of at least 40 mL/min/1.73 m2). The LVM index was estimated by indexing LVM to height(2.7). Sixteen patients had a cadaveric transplant and seven had a live donor transplant; the mean duration between the two studies was 1.9 +/- 1.6 yr; and the mean GFR was 55.0 +/- 21.4 mL/min/1.73 m2. There was no significant difference in the mean values of the LVM index while on dialysis and after renal Tx (43.9 +/- 17.8 g/m2.7 and 39.3 +/- 12.0 g/m2.7, respectively, p = 0.19), or in the prevalence of LVH (52% and 56%, respectively). Interval changes in the LVM index in individual subjects between the two studies were significantly associated with interval changes in indexed systolic (r = 0.42, p = 0.04) and diastolic (r = 0.42, p = 0.05) blood pressures. Interval changes in hemoglobin, blood urea nitrogen (BUN), creatinine, and duration after Tx did not correlate with changes in the LVM index. There was no significant difference in LVM index change according to the type of dialysis, donor source, and the cause of renal failure. In multivariate analysis, the baseline LVM index and changes in indexed SBP were independent predictors for LVM index change after renal Tx. We conclude that LVH persists in children and adolescents after renal Tx. Control of blood pressure might be an important factor in regression or prevention of progression of LVH in these patients.

Evolution of Left Ventricular Hypertrophy and Function During Long-Term Treatment of Systemic Hypertension With Enalapril

Continued treatment of hypertensive patients with enalapril reduced left ventricular (LV) hypertrophy steadily over a period of 5 years (by which time gross structural parameters were normal) and produced no further reduction during the following 2 years. Temporary suspension of treatment after 5-year follow-up gave rise to an increase in blood pressure, and to deterioration of LV isovolumic relaxation time and deceleration of the ventricular filling E wave, both of which chiefly reflect the active relaxation of the ventricle.