Regression of left ventricular hypertrophy: Are there preferred drugs?

The presence of left ventricular hypertrophy (LVH) confers markedly increased risk of cardiovascular morbidity and mortality in patients with hypertension. Regression of left ventricular (LV) mass with antihypertensive therapy is associated with reduction in cardiovascular events. In studies based on monotherapy, among the classes of antihypertensive drugs that have been adequately tested, diuretics and angiotensin-converting enzyme inhibitors appear to be the most effective agents for reducing LV mass. New avenues of research, based on combination antihypertensive therapy and on a more sophisticated understanding of the molecular mechanisms of LVH, may yield new pharmacologic approaches to regressing LV mass.     

Mitochondria and left ventricular hypertrophy

Introduction Left ventricular hypertrophy (LVH) is one of the vi-cious organ damages of essential hypertension. It contrib-utes a lot to high mortality of essential hypertension due tosudden cardiac death, ventricular arrhythmia and heart     

Electrocardiography–left ventricular mass discrepancies in left ventricular hypertrophy: electrocardiography imperfection or beyond perfection?

The problem of discrepancies between left ventricular mass (LVM) and electrocardiography (ECG) findings in diagnosis of left ventricular hypertrophy (LVH) is approached from the perspective of the diagnostic ability of ECG. Contrary to current clinical understanding of LVH as an increase in LVM, the LVH is defined as the organ manifestation of the hypertrophic growth of cardiomyocytes accompanied by changes in interstitium. This complex understanding of the hypertrophic rebuilding of LV myocardium in LVH is the crucial requirement to understand the role of ECG in LVH diagnosis. The basic statements of the article are based on the fact that ECG provides information on the electrical field generated by the heart; therefore,

• ECG cannot be a surrogate method for the LVM estimation by its nature. The hypothesis that the ECG estimates LVM requires modification for the additional effects of myocardial tissue changes and conduction on the ECG.

• The added value of ECG in LVH diagnosis is given by its ability to register the electrical field of the heart and thus to estimate the electrical status of the myocardium.

Are all mutant SNARES equal?

In this issue of Blood, Pagel et al carefully deliniate some fascinating phenotype/genotype correlations in a larger cohort than in their earlier reports of familial hemophagocytic lymphohistiocytosis (HLH).     

Does a prolonged QT peak identify left ventricular hypertrophy in hypertension?

BACKGROUND: Left ventricular hypertrophy is a powerful predictor of death. Hypertensive subjects with left ventricular hypertrophy can have increased QT (end) dispersion, which is associated with cardiac death. Despite its prognostic value, QT (end) dispersion is not widely used. QTp (i.e. start of QRS to peak of T wave) is easier to measure. Therefore, we tested the hypothesis that long QT peak was associated with left ventricular hypertrophy and assessed its cost-effectiveness at diagnosing left ventricular hypertrophy. METHODS: ECGs and echocardiograms were recorded in 47 hypertensive patients. The onset of the QRS complex and peak of T wave of lead I of each subject's ECGs were digitised by one observer blind to results of the echocardiogram. Receiver-operator characteristics curves were plotted to determine the sensitivity and specificity of different cut-off values of QT peak at predicting left ventricular hypertrophy (defined as left ventricular mass index> or =134 g/m2 in male, > or =110 g/m2 in female). RESULTS: The heart-rate corrected QT peak of lead I correlated with left ventricular mass index (r=0.45, P=0.002). If all patients with a prolonged QT peak (> or =300 ms) had an echocardiogram, then no cases of left ventricular hypertrophy would be missed (100% sensitive). This novel ECG criterion not only had better positive and negative predictive values than the Sokolow-Lyon voltage criteria, but also resulted in more cost-effective resource use (< pound 370 vs. pound 1750/case of left ventricular hypertrophy detected). CONCLUSION: If the results of this small pilot study are confirmed in larger studies, then measuring QT peak of lead I may become a cost-effective way of identifying hypertensives who are likely to have echocardiographic left ventricular hypertrophy.     

Mild left ventricular hypertrophy in essential hypertension: is it really arrhythmogenic?

Left ventricular hypertrophy (LVH) has been associated with an increased incidence of ventricular arrhythmias and sudden cardiac death in hypertensive patients. However, it is not known whether this relationship exists in early asymptomatic hypertensives with mild LVH. We prospectively examined 100 consecutive patients with essential hypertension, 35 without and 65 with mild LVH on echocardiography. All underwent a detailed noninvasive arrhythmia work-up and were subsequently followed-up for 3 ± 1 years in an ambulatory hypertension clinic. None of the 12-lead electrocardiographic parameters examined differed between the two hypertensive groups. A similarly low incidence of simple forms of ventricular ectopy was present in both groups, whereas complex forms of ventricular ectopy were extremely rare in either group. The signal-averaged electrocardiographic parameters examined were also not significantly affected by the presence of mild LVH. Arrhythmia-related symptoms or malignant ventricular arrhythmia events were not observed in either group of patients during follow-up with antihypertensive treatment. The latter resulted in LVH regression in the 65 patients with mild LVH at baseline. It appears that mild LVH among ambulatory hypertensive patients does not carry an additive arrhythmogenic risk and can be successfully reversed with the appropriate antihypertensive therapy, with no need of additional antiarrhythmic management.     

Are all calories created equal? Emerging issues in weight management

The global prevalence of overweight and obesity is growing. Correction of the problem through dietary intervention has been disappointing and has prompted research into variations of diet composition or pattern to promote negative energy balance. Limited research suggests that selected approaches, such as low-carbohydrate diets, augment weight loss and offer an advantage over conventional low-fat diets. This has led to the hypothesis that although in theoretical terms a calorie is a calorie, in practice this is not the case. Support for such views and plausible mechanisms exist. Although any advantage may augment weight management, reported discrepancies between theoretical and observed effects are small. Thus, energy-restricted diets should be based primarily on energy intake and expenditure.     

Fork in the road: Are all bifurcations created equal?

• The TRYTON study evaluated routine side branch (SB) stenting with a novel bare metal stent (BMS) designed for true bifurcation lesions (Medina 1,1,1; 1,0,1; 0,1,1) and compared it to a strategy of balloon angioplasty with provisional stenting. It failed to meet the primary endpoint of non‐inferiority in target vessel failure mainly driven by peri‐procedural myocardial infarction (MI) with elevated CK‐MB > 3× the upper limit of normal.
• In this substudy, 41% of patients who had a SB diameter > 2.25 mm were evaluated and the new stent was found to be non‐inferior in the primary outcome of target vessel failure with no difference in post‐procedural MI.
• This substudy suggests that appropriately sized SB stents with TRYTON may be useful when the SB is >2.25 mm in diameter. However, further studies could evaluate routine use of FFR for SBs; drug eluting versions of the stent as well as stents designed for vessels 2.25 mm in diameter which are frequently felt to be clinically larger when not subjected to core lab analysis.

     

Electrical remodeling in left ventricular hypertrophy—is there a unifying hypothesis for the variety of electrocardiographic criteria for the diagnosis of left ventricular hypertrophy?

Although electrocardiography has been used to estimate left ventricular hypertrophy and to obtain useful prognostic information in different clinical settings, its correlation with left ventricular mass is poor and, therefore, its sensitivity and specificity for the diagnosis of left ventricylar hypertrophy are low. Experimental work has demonstrated that the increase in voltage and duration of the QRS complex of the electrocardiogram are not only related to left ventricular mass but also to changes in the electrophysiological properties of the myocardium. Therefore, a new strategy is needed to use electrocardiography not to estimate left ventricular mass but aimed to add useful prognostic information.     

Renal protection: Are all antihypertensive drugs comparable?

Chronic kidney disease, stage 3 or higher, affects approximately 20 million people in the United States. Aggressive management of blood pressure is critical to slow the decline in renal function. Despite adequate control, however, patients continue to progress to end-stage renal disease. A surrogate marker for renal parenchymal injury is the presence of proteinuria. Blood pressure reduction per se has been shown to decrease proteinuria. However, certain classes of antihypertensive agents, namely the inhibitors of the renin-angiotensin-aldosterone system, exert antiproteinuric and renoprotective effects that are in addition to, but independent of, blood pressure lowering. This article reviews the beneficial renoprotective effects of various classes of antihypertensive agents in chronic kidney disease.