Monitoring of antihypertensive therapy for reduction in left ventricular mass

BACKGROUND: Pressure pulse waveform features may predict treatment-induced regression of left ventricular (LV) mass better than casual brachial blood pressure (BP). We compared predictive power for LV mass reduction between the putative optimal pulse waveform feature (pulse amplification) and the putative optimal brachial cuff measurement (self BP monitoring at home). METHODS: Forty-three patients with hypertension received standard medical treatment for 1 year. Self BP monitoring was used to determine home morning and evening BPs. Radial pressure waveforms recorded with applanation tonometry in the clinic were transformed to aortic waveforms, and pulse amplification (upper limb pulse pressure/central pulse pressure) was calculated. RESULTS: Antihypertensive therapy significantly (P < .05) reduced LV load, manifest by a decrease in both home BPs and by an increase in amplification. These changes were accompanied by significant reduction in echocardiographically determined LV mass index (LVMI). However, treatment-induced LVMI change did not correlate with change in any component of home BPs, but closely correlated with change in amplification (r = -0.54, P < .001). Amplification was a strong determinant of LVMI reduction, independent of age, gender, and home BP. Estimated subject numbers required for predicting a significant LVMI reduction were far less when the pulse waves were used rather than home BP; for alpha = 0.05 and beta = 0.20, numbers were 25 subjects for amplification but more than 1000 for home BP. CONCLUSIONS: Regression of LV mass is closely associated with reduction in wave reflection, and can be assessed more precisely and easily from radial tonometry than use of the brachial cuff measurement, even in the home setting.     

Increased left ventricular mass is not associated with impaired left ventricular diastolic filling in normal individuals

BACKGROUND: Hypertensive left ventricular (LV) hypertrophy has been associated with diastolic dysfunction. However, the underlying physiological relationship between LV size and diastolic function remains to be clarified. The aim of this study was to evaluate the relationship between several measures of diastolic filling and LV mass in a population sample. METHODS: We used M-mode and Doppler echocardiography to compare left ventricular mass index (LVMI) and wall thickness with five measures of ventricular diastolic filling (ratio of the peak early mitral inflow velocity to the peak atrial mitral inflow velocity, deceleration time of early mitral inflow, isovolumetric relaxation time, ratio of the peak pulmonary venous systolic to diastolic flow and difference between the durations of the pulmonary venous and mitral inflow atrial waves) in 159 healthy volunteers. RESULTS: LVMI was significantly (P< 0.0001) greater in men (81.3 g/m2, interquartile range: 67-94) than women (59.7 g/m2, interquartile range: 49-74), but no gender differences were observed in diastolic filling. Higher age, blood pressure and heart rate showed significant correlation with diminished diastolic filling. However, no measure of diastolic filling correlated with LVMI or wall thickness in either univariate or multiple regression analyses that adjusted for relevant covariates. CONCLUSIONS: LVMI does not explain physiological differences in diastolic filling. The significant decline in diastolic filling with age reflects changes in the quality rather than the quantity of myocardial tissue.     

Improved left ventricular filling accompanies reduced left ventricular mass during therapy of essential hypertension

Abnormal left ventricular diastolic performance, an early manifestation of hypertension in the heart, may precede the development of left ventricular hypertrophy. To assess effects of antihypertensive therapy on the heart, left ventricular mass (determined by echocardiography) and rapid left ventricular filling rate (determined by radionuclide ventriculography) were compared before and after 6 months of treatment of 16 patients. Nitrendipine (a dihydropyridine calcium channel blocker) was given alone or in combination with either propranolol or hydrochlorothiazide, or both, and significantly reduced blood pressure (156/103 +/- 12/7 to 137/89 +/- 10/6 mm Hg). In 6 of the 16 patients, left ventricular mass decreased by more than 10% (270 +/- 95 to 193 +/- 47 g, p less than 0.01); in the same patients, left ventricular filling rate increased (2.03 +/- 0.35 to 2.30 +/- 0.45 end-diastolic counts/s [EDC/s], p less than 0.01). In the one patient whose left ventricular mass increased (137 to 195 g), left ventricular filling rate decreased from 2.01 to 1.78 EDC/s. In the remaining nine patients who had no change in left ventricular mass, there was no significant changes in left ventricular filling. The changes in ventricular mass and filling could not be related to the extent of change in blood pressure or heart rate. These data suggest that regression of left ventricular mass during antihypertensive therapy with nitrendipine is accompanied by improved diastolic function.     

Regression of left ventricular hypertrophy and improvement of its diastolic function in patients with arterial hypertension under influence of antihypertensive therapy

Antihypertensive therapy with sequential addition of drugs (noliprel, noliprel-forte, metoprolol, amlodipine) for achievement of target blood pressure (BP) below 140/90 mm Hg was used in the treatment of 99 patients with arterial hypertension (AH) with (n=51) or without left ventricular (LV) hypertrophy (LVH). At initial Doppler study of transmitral blood flow all patient with LVH had type 1 (n=48) or type 2 (n=3) diastolic LV dysfunction. Among patients without LVH 13 had minor type 1 diastolic LV dysfunction. After 12 - 14 months of antihypertensive therapy in all 44 patients with moderate LVH (myocardial mass index below 140 g/m2) BP corresponded to target level. This was associated with 6% decrease of myocardial mass index (MMI) and its normalization in 2/3 of patients, restoration of diastolic function in 3/4 of patients and its improvement in other patients, decrease of functional class, in rease of 6 min walking distance, and improvement of quality of life according to questionnaire for patients with CHF. In 7 patients with pronounced LVH (MMI 140 g/m2) target BP was not achieved, LVMMI, diastolic function, and functional class did not change, however tolerance to physical effort and quality of life improved. Thus in all patients with AH without LVH target BP level was achieved. In minor initial diastolic dysfunction diastolic function restored to normality, functional class, tolerance to physical work and quality of life improved.     

Regression of left ventricular hypertrophy during antihypertensive treatment

Left ventricular hypertrophy is a risk factor for cardiovascular events and stroke. It has been demonstrated that the regression of left ventricular hypertrophy (evaluated by 12-lead electrocardiography and by echocardiography) during antihypertensive treatment is associated with a lower risk of cardiovascular mortality and may thus improve the prognosis. Black people run a disproportionately high risk of developing essential arterial hypertension which frequently results in end organ damage, including left ventricular hypertrophy, haemorrhagic stroke and renal failure. We report a case of significant regression of left ventricular hypertrophy in a sub-Saharan African patient, during antihypertensive treatment.     

Effectiveness of the antihypertensive action of lisinopril on left ventricular mass and diastolic filling.

The effect of antihypertensive treatment with lisinopril (10 to 20 mg) on left ventricular mass and diastolic function was studied in 35 patients with mild to moderate hypertension. At baseline 6 and 12 months after treatment responders to lisinopril were examined by complete echo Doppler in order to measure left ventricular mass, diastolic and systolic function. Only 30 patients concluded the study follow-up. Lisinopril successfully reduced mean blood pressure (from 122 +/- 10 to 110 +/- 11 mmHg), without modification in heart rate, and left ventricular mass index (from 145 +/- 57 to 116 +/- 42 g.m-2) at month 6, with mild additional reduction at month 12. Isovolumic relaxation time was reduced but still abnormal at months 6 and 12, whereas deceleration time significantly changed only (from 230 +/- 40 to 195 +/- 35 msec) at month 12. Our results indicate that lisinopril is more successful in reducing left ventricular mass than in improving diastolic filling.     

Apropos of acute changes in left ventricular filling induced by antihypertensive treatment]

The purpose of the study was to interpret the acute improvement in left ventricular (LV) filling induced by a new calcium channel blocker (SR 33 557) using Doppler echocardiography. Thirteen patients, 29 to 68 years old (mean 52) with mild to moderate hypertension were examined by Doppler echocardiography before and 4 hours after treatment (SR 33 557: 300 mg). The LV filling parameters, E, A, A/E, VTIM, VTIA, VTIA/VTIM, pressure half time (PHT) and isovolumic relaxation time (IRT) were measured. An index of left atrial pressure was obtained by measuring the mean pulmonary arterial pressure (PAP). The following hemodynamic parameters were also obtained: systolic blood pressure (SBP), heart rate (HR), PR interval (PR), stroke volume (SV) at aortic origin, total systemic resistances (TSR), pulse wave velocity (PWV) at thoracic descending aorta, LV end systolic stress (ESS), LV geometry (thickness/radius: th/r) and systolic function indices: mean VCF and contractility (mean VCF-ESS relationship). Following acute treatment, E and VTIM increased, A, VTIA and PHT did not change, and A/E, VTIA/VTIM ans IRT decreased, both significantly (p < 0.05). PAP did not change, HR, SBP, TSR, PWV, ESS decreased and PR increased both significantly (p < 0.05). LV geometry and systolic function did not change. No significant relationship was found between LV filling changes and changes in hemodynamic parameters. In conclusion, the acute increase in early LV filling induced by the calcium blocker treatment may be interpreted as the consequence of the improvement in LV relaxation in the absence of any change in left atrial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)     

Regression of left ventricular mass with captopril and metoprolol, and the effects on glucose and lipid metabolism

Objective: Angiotensin II and insulin have been suggested to promote the development of hypertensive left ventricular (LV) hypertrophy. We compared the effects of captopril and metoprolol on the regression of LV mass and the relation to insulin sensitivity.Design:     

Regression of left ventricular hypertrophy during long-term antihypertensive treatment--a comparison between felodipine and the combination of felodipine and metoprolol.

Seventy-six hypertensive patients with left ventricular hypertrophy (LVH) were randomized to receive felodipine or felodipine plus metoprolol in a double-blind parallel-group study. The doses of each treatment regimen were titrated to obtain a diastolic blood pressure (BP) of less than 95 mmHg. The duration of the treatment was 9 months. At the end of the study, BP was significantly reduced in both groups, and the reduction did not differ between the groups. Left ventricular posterior wall and septum thickness were significantly and similarly reduced in both groups. Left ventricular systolic and diastolic end diameters were not significantly changed. Left ventricular mass (LVM) was significantly and similarly reduced in both treatment groups, as was the ratio of LVM and left ventricular end diastolic volume. In conclusion, felodipine and the combination of felodipine and metoprolol reduced left ventricular hypertrophy to the same extent when BP was similarly reduced.     

Altered left ventricular diastolic filling following a marathon is a reproducible phenomenon

The present study examined the reproducibility of alterations in left ventricular function and cardiac biomarkers in a cohort of athletes following two marathons, one year apart. Eight participants in the 2004 and 2005 London Marathons were tested pre- and post-race via echocardiography and humoral analysis. Reductions in diastolic filling, unrelated to loading or heart rate, following both marathons were reproducible within individuals, which may be a function of exercise duration. In contrast, exercise-induced cardiac troponin release was inconsistent.     

Effect of antihypertensive monotherapy and combination therapy on arterial distensibility and left ventricular mass

BACKGROUND: Angiotensin-converting enzyme (ACE) inhibitors and calcium channel blockers (CCBs) increase arterial compliance and decrease left ventricular mass in hypertensive patients. This study examined whether combined therapy has greater arterial and cardiac effects than doubled doses of the individual drugs. METHODS: This prospective, randomized, open-label study enrolled 106 patients aged >/=18 years with mild-to-moderate hypertension. Patients were randomized to 5 mg of amlodipine or 20 mg of benazepril for 2 weeks; then, depending on randomization assignment, they were force-titrated to 10 mg of amlodipine or 40 mg of benazepril monotherapy, or to combination amlodipine (5 mg) and benazepril (20 mg) treatment for 22 weeks. Arterial distensibility was assessed using the DynaPulse ambulatory system, and left ventricular mass was assessed by echocardiography. RESULTS: Combination therapy (0.71% +/- 0.51% mL/mm Hg) increased arterial distensibility more than amlodipine (0.28% +/- 0.69% mL/mm Hg; P =.008) or benazepril (0.39% +/- 0.62% mL/mm Hg; P =.03) monotherapies. Left ventricular mass decreased more with combination treatment (65 +/- 56 g) than with amlodipine (28 +/- 4 g; P <.02); the difference from benazepril (42 +/- 50 g) was not significant. CONCLUSIONS: Combined ACE inhibitor and CCB treatment was more efficacious than high doses of the individual agents in increasing arterial compliance and reducing left ventricular mass. These findings indicate that appropriately selected combinations of antihypertensive drugs might have enhanced cardioprotective effects.     

Impaired left ventricular rapid filling during exercise in patients with hypertrophic cardiomyopathy

The influence of exercise on left ventricular diastolic filling was evaluated in 14 patients with hypertrophic cardiomyopathy (HCM) and 14 normal controls (NC) by dynamic exercise echocardiography. Using X-Y digitizer and computer, normalized peak rate of change of the left ventricular dimension during systole (pVs) and the rapid filling phase (pVd) were determined from the left ventricular echocardiograms at rest and during exercise when heart rate reached 100 beats/min. At rest and during exercise, pVs was significantly higher in HCM (3.2 +/- 0.4/s at rest, 4.3 +/- 1.4/s during exercise) than in NC (2.4 +/- 0.5/s at rest, 3.0 +/- 0.4s during exercise) (p less than 0.001, p less than 0.001, respectively), but pVd in HCM (4.2 +/- 1.0/s at rest, 5.8 +/- 1.0/s during exercise) was not significantly different from that in NC (4.1 +/- 1.0/s at rest, 6.0 +/- 0.7/s during exercise). The ratio of pVd to pVs (pVd/pVs) in HCM did not show significant increment during exercise (1.35 +/- 0.38 to 1.43 +/- 0.35), though that ratio in NC was significantly increased by exercise (1.67 +/- 0.22/s to 1.97 +/- 0.19/s, p less than 0.001). There was no correlation between pVd and the degree of left ventricular hypertrophy. These results suggest that diastolic reserve to exercise is depressed in HCM and that other factors besides left ventricular hypertrophy may account for diastolic abnormality.     

Regression of left ventricular mass in systemic hypertension.

The importance of treatment in systemic hypertension and cardiovascular morbidity and mortality has been established. Although systemic hypertension is the most important factor in the pathogenesis of left ventricular hypertrophy, other factors such as catecholamines and renin-angiotensin system may be involved. Increased left ventricular mass causes reduction in coronary reserve and may lead to acute ischemic events. Equally efficacious antihypertensive agents may have diverse effects on left ventricular hypertrophy and left ventricular function. New tomographic techniques with improved spatial resolution are emerging in the evaluation of left ventricular mass and may therefore provide better assessment of changes in left ventricular mass. With improved measures of left ventricular mass the question as to whether regression of left ventricular mass provides an additional benefit beyond control of blood pressure in hypertensive individuals may be finally answered.     

Regression of left ventricular hypertrophy--are there differences between antihypertensive agents?

Echocardiographically determined left ventricular mass (LVM) is currently considered to be the most powerful risk indicator for cardiovascular disease, yielding prognostic information beyond that provided by the evaluation of traditional cardiovascular risk factors, high blood pressure included. It has been considered logical to try to obtain regression of cardiac hypertrophy, even though the risk-reducing implications of such a measure remain to be fully established. Experimental and clinical studies have shown that some classes of antihypertensive compounds are less effective than others in causing reversal of left ventricular hypertrophy (LVH) in spite of being similarly efficacious in lowering blood pressure. In order to extract the maximum amount of information from clinical studies, a meta-analysis was performed. This analysis included 109 treatment studies, each conformed to strict present rules. Only studies with pharmacological antihypertensive therapy and echocardiographically determined LVM were included. An analysis of the effect of the four first-hand antihypertensive treatment principles, adjusted for differences between studies with ANCOVA, showed that the ACE inhibitors, beta-blockers and calcium antagonists all reduce LVM by reversing wall hypertrophy and that the effect is most pronounced with ACE inhibitors. Diuretics reduce LVM mainly by a reduction in left ventricular diameter. If the difference in ability to reverse LVH, between ACE inhibitors and beta-blockers/diuretics would correspond to a difference in prognosis, then the outcome of antihypertensive therapy might be expected to improve. This hypothesis is currently under investigation.     

Regression of left ventricular hypertrophy in hypertensive patients: responses to exercise by antihypertensive treatment

The effects of various antihypertensive treatments on the echocardiographic and electrocardiographic findings of left ventricular (LV) hypertrophy were studied in 75 patients with essential hypertension. The hemodynamic effects of the therapy during exercise were also compared. LV mass by echocardiogram was significantly reduced by beta-blockade and angiotensin converting enzyme inhibition (ACEI), but only slightly reduced by Ca channel blockade. QRS high voltage criteria of LV hypertrophy by electrocardiogram were reduced by all 3 of these antihypertensive treatments. At submaximal exercise, the pressor responses were attenuated by captopril, but not influenced by metoprolol or nifedipine. The increase in plasma norepinephrine by exercise was significantly suppressed after captopril, but was somewhat augmented after metoprolol or nifedipine. These observations indicate that the responses of hemodynamics and sympathetic nervous activity to exercise are different after the treatment by beta-blocker, Ca channel blocker or ACEI, in spite of the equal antihypertensive effect. However, it is suggested that the regression of LV hypertrophy might be induced by antihypertensive therapy, though the different grade by the individual drug.     

The effect of chronic antihypertensive therapy on the index of left ventricular mass in patients with essential hypertension

M-mode echocardiography was used in 80 patients with essential hypertension to study changes in the index of left ventricular mass during treatment over 3 years with reserpine, prazosin, indapamide and atenolol, separately or in combination. Forty patients completed a follow-up period of 36 months, while 5 patients died during this period. In all 5 groups, the index of left ventricular mass decreased significantly from the baseline after 1 and 3 years of treatment, except in those patients receiving prazosin in which there was no significant difference in the index of left ventricular mass between 1 and 3 years of treatment. Our results confirm that effective treatment of blood pressure results in a significant reduction in the index of left ventricular mass. Furthermore, this reduction was seen with all modes of treatment and suggests that it was reduction of blood pressure rather than any specific pharmacological property of the drugs that was of major importance.     

Reversibility of left ventricular hypertrophy by differing types of antihypertensive therapy.

Left ventricular hypertrophy (LVH), as assessed by ECG or echocardiography, is a powerful independent coronary risk factor. The present overview of 104 studies sets out to compare the ability of various forms of antihypertensive therapy to reverse LVH as assessed by echocardiography. Most observations involved four classes of treatment--combination therapy, ACE inhibitors, beta-blockers and calcium antagonists (mainly dihydropyridines). The former two therapies were significantly more effective than the latter two in reversing LV mass, independently of length of time on treatment and degree of fall in blood pressure. Possible reasons for these differences are discussed. The clinical significance of these results is unclear although preliminary data indicate that regressing LVH is associated with fewer cardiovascular events.