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Different pathophysiology of cardiac hypertrophy in hypertension and hypertrophic cardiomyopathy
Insights
Cardiac hypertrophy mechanisms differ between hypertension and hypertrophic cardiomyopathy. Angiotensin-converting enzyme inhibitor treatment regressed hypertrophy in hypertension but not in cardiomyopathy, indicating distinct pathophysiologies.
Area of Science:
- Cardiology
- Molecular Biology
- Pharmacology
Background:
- Cardiac hypertrophy, an enlargement of the heart muscle, can arise from various conditions.
- Understanding the underlying pathophysiology is crucial for effective treatment strategies.
- Arterial hypertension and hypertrophic cardiomyopathy represent distinct causes of cardiac hypertrophy.
Purpose of the Study:
- To investigate the differences in cardiac myocyte DNA synthesis and cell cycle progression in patients with arterial hypertension versus hypertrophic cardiomyopathy.
- To evaluate the efficacy of long-term angiotensin-converting enzyme (ACE) inhibitor therapy in regressing cardiac hypertrophy in these two patient groups.
Main Methods:
- DNA synthesis and cell cycle phases (G2M) were analyzed using flow cytometry on autopsy-derived myocardial tissue from 10 hypertensive and 10 cardiomyopathic patients.
- Twenty hypertensive patients and 15 hypertrophic cardiomyopathy patients received 12 months of captopril (an ACE inhibitor).
- Cardiac hypertrophy regression was assessed via echocardiography, measuring left ventricular mass before and after treatment.
Main Results:
- Myocardium from hypertrophic cardiomyopathy patients showed a significantly lower percentage of cells in the G2M phase compared to hypertensive patients (1.1% vs. 7.7%).
- Captopril treatment led to significant regression of left ventricular mass in hypertensive patients (234g to 198g, P<0.01).
- No significant reduction in left ventricular mass was observed in hypertrophic cardiomyopathy patients treated with captopril (305g to 285g).
Conclusions:
- The mechanisms driving cardiac hypertrophy differ significantly between arterial hypertension and hypertrophic cardiomyopathy.
- ACE inhibition is effective in reversing cardiac hypertrophy associated with hypertension, but not that caused by hypertrophic cardiomyopathy.
- These findings underscore the importance of differentiating the etiology of cardiac hypertrophy for targeted therapeutic interventions.
Abstract:
In order to investigate differences in the pathophysiology of cardiac hypertrophy between patients with arterial hypertension and hypertrophic cardiomyopathy, DNA synthesis by cardiac myocytes and the effects of an angiotensin-converting enzyme inhibitor were examined in these two groups of patients. DNA synthesis and the cell cycle were investigated by flow cytometry using autopsy materials from patients with hypertension and hypertrophic cardiomyopathy. The hypertension group (n=10) included four men and six women aged 61+/-10 years (heart weight: 470+/-79 g, mean+/-s.d.); the cardiomyopathic group (n=10) included eight men and two women aged 61+/-23 years (heart weight: 615+/-211 g). The percentage of cells in G2M phase of the cell cycle was significantly decreased in the myocardium from patients with hypertrophic cardiomyopathy compared with that from hypertensive patients (cardiomyopathy v hypertension: 1.1+/-0.6 v 7.7+/-2.6%, mean+/-s.d.). Captopril, an angiotensin-converting enzyme inhibitor, was administered for 12 months to patients with hypertension (n=20) and hypertrophic cardiomyopathy (n=15). Regression of cardiac hypertrophy was assessed by echocardiography. Long-term administration of captopril achieved regression of cardiac hypertrophy in the hypertensive patients, but not in the patients with hypertrophic cardiomyopathy. In the hypertensive patients, the left ventricular mass was 234+/-9 g before treatment and 198+/-26 g after treatment (mean+/-s.d., P<0. 01). In cardiomyopathic patients, on the other hand, there was no significant difference of left ventricular mass after treatment (before v after, 305+/-85 v 285+/-90 g, mean+/-s.d.). These results suggest that the mechanism of cardiac hypertrophy differs between patients with hypertension and hypertrophic cardiomyopathy.