Distribution of dyssynchrony in subjects with no known cardiac disease and comparison of velocity vector imaging to color-coded tissue Doppler imaging.

Data on the distribution of dyssynchrony in subjects with normal ejection fraction (EF) and normal QRS are scarce. We studied 100 subjects with no known cardiac disease (52% male, mean age 60 ± 17 years) using velocity vector imaging (VVI). Seventeen percent had septal to lateral (S-L) wall longitudinal delay >75 msec, 63% of subjects had S-L wall radial delay >75 msec, and 25% had a circumferential opposing wall delay >100 msec. Those with circumferential opposing wall delay of >100 msec had a lower EF (57 ± 5% vs. 62 ± 5%, P < 0.05). In an additional group of 33 patients, we compared the longitudinal dyssynchrony parameters as assessed by VVI and tissue Doppler imaging (TDI) and found them to be comparable. In conclusion, we find significant variation in time to peak velocities in subjects with no known cardiac disease, who had a normal left ventricular ejection fraction and QRS duration. VVI is comparable to TDI.

Dyssynchrony in obese subjects without a history of cardiac disease using velocity vector imaging.

BACKGROUND: The aim of this study was to examine the occurrence of intra-left ventricular (LV) dyssynchrony in obese versus nonobese subjects without known cardiac disease using Velocity Vector Imaging (VVI). METHODS: One hundred ninety consecutive subjects with no known cardiac disease had their echocardiograms analyzed using VVI after excluding subjects with QRS durations>120 msec or LV ejection fractions<55%. Study subjects were divided into two groups on the basis of body mass index: obese (>30 kg/m2) and nonobese (<30 kg/m2). RESULTS: The final cohort included 136 subjects (74 obese; 32% women; mean age, 55±16 years). The occurrence of intra-LV dyssynchrony was higher in the obese group compared with the nonobese group. CONCLUSIONS: There was an increased prevalence of intra-LV dyssynchrony in obese subjects, especially longitudinal and radial dyssynchrony. This dyssynchrony may signal a mechanism by which obesity predisposes to the development of heart failure.

Discrepancy between gradients derived by cardiac catheterization and by Doppler echocardiography in aortic stenosis: how often does pressure recovery play a role?

Studies have shown very good correlation between Doppler-derived gradients and gradients obtained by cardiac catheterization (cath) in aortic stenosis (AS). However, the phenomenon of pressure recovery may lead to significant overestimation of aortic valve (AV) gradients by Doppler echocardiography (echo). We hypothesized that echo-derived gradients will be higher in mild-moderate AS because of pressure recovery. We studied 94 patients who had echo and cardiac caths in a span of 1 week. The mean age was 72 +/- 13 years, 54% males, 79% had coronary artery disease, and the mean left ventricular ejection fraction was 45 +/- 22%. The mean cardiac output and cardiac indices were 5.1 +/- 1.4/2.7 +/- 0.6 (l/mt), (l/m(2)), respectively. For those with mild AS, echo overestimated gradients in 9.5% of patients (4/42) by an average of 19 mmHg, thus misclassifying the degree of stenosis. In those with moderate AS, 14% (3/21) were misclassified as severe AS (gradient overestimation by an average of 13.6 mmHg). In those with severe AS, echo underestimated gradients in 13% (4/31) by an average of 22.7 mmHg. The aorta at the sinotubular junction was 2.8 cm in those patients with mild AS in whom gradients were overestimated by more than 20 mmHg compared to a sinotubular junction diameter of 3.12 cm in those with mild AS and no overestimation of gradients. The AV area/aortic root ratio was 0.4 in those with mild AS and 0.2 in those with severe AS (P < 0.05).

Aldosterone receptor antagonists in the medical management of chronic heart failure.

The benefits of aldosterone receptor antagonists (spironolactone and eplerenone) for patients with heart failure were shown in 2 recent randomized controlled trials. Some of the proposed mechanisms of action of aldosterone antagonists are (1) inhibition of myocardial and vascular remodeling, (2) blood pressure reduction, (3) decreased collagen deposition, (4) decreased myocardial stiffness, (5) prevention of hypokalemia and arrhythmia, (6) modulation of nitric oxide synthesis, and (7) immunomodulation. Like many hormone receptors, the aldosterone receptor can be either nuclear or membrane bound. Most of the activities of the aldosterone receptor are subserved by the nuclear receptors and often lead to alterations in gene transcription. Although these agents are well tolerated in carefully selected patient populations that meet the inclusion criteria of large clinical trials, their use in unselected elderly patients with heart failure and multiple comorbidities has been associated with a significant risk of hyperkalemia and renal failure. Although no convincing data exist to predict which individual patients will respond to aldosterone inhibition, patients with more severe heart failure and those with acute myocardial infarction with concomitant heart failure or left ventricular dysfunction are most likely to respond. Theoretically, aldosterone receptor antagonists may also be beneficial in patients with more mild to moderate systolic heart failure or even in those with diastolic heart failure, although direct evidence is still lacking.

Why do patients fail to receive beta-blockers for chronic heart failure over time? A "real-world" single-center, 2-year follow-up experience of beta-blocker therapy in patients with chronic heart failure.

BACKGROUND: The longitudinal pattern of beta-blocker use in a heart-failure practice setting has not been explored. Previous studies have not specifically addressed the use of beta-blockers over time to determine the rate of use and reasons for discontinuation. The long-term compliance rate for beta-blocker drugs outside the context of a clinical trial has not been established. METHODS: We prospectively followed a cohort of 500 consecutive patients between March and May 2001, with a clinical diagnosis of chronic heart failure seen in a specialized heart failure clinic and determined the longitudinal pattern of beta-blocker use and clinical outcomes over a 2-year period. RESULTS: The final cohort consists of 340 patients with a complete 2-year follow-up data (mean age 61 +/- 14 years, 69% men, 53% with ischemic etiology, mean ejection fraction 27.6 +/- 15%). At 6, 12, and 24 months, beta-blocker utilization rates were maintained in 69%, 70%, and 74% of patients, respectively. Of the 120 confirmed initial non-beta-blocker users, 28 (23%) were subsequently started on beta-blocker, despite suspected relative contraindications in 53% of patients. Over a period of 2 years, the discontinuation rate was 10%, with failure to restart a beta-blocker after hospitalization as the most common reason for beta-blocker discontinuation. CONCLUSION: Utilization rates of beta-blockers in our heart failure clinic have remained constant at approximately 70% throughout a 2-year follow-up. Of those who discontinued beta-blockers (10%), the most common documented cause was failure to restart beta-blockers after hospitalization.