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Therapy of hypertensive cardiac hypertrophy and impaired coronary microcirculation
1Medical Clinic B, Heinrich-Heine University of Düsseldorf, Germany.
Insights
Antihypertensive treatments may repair cardiac remodeling and improve coronary flow reserve in hypertension. Further research is needed to determine if improvements stem from myocardial factors or microcirculation repair.
Area of Science:
- Cardiovascular Medicine
- Pharmacology
- Hypertension Research
Background:
- Arterial hypertension causes cardiac remodeling, including myocyte hypertrophy, fibrosis, and coronary microcirculation dysfunction.
- This remodeling leads to left ventricular dysfunction and impaired coronary flow reserve.
- Effective antihypertensive therapy should address cardiac remodeling and normalize blood pressure.
Purpose of the Study:
- To investigate the impact of antihypertensive treatments on repairing hypertensive cardiac remodeling.
- To assess the ability of these therapies to restore coronary microcirculation and improve coronary flow reserve.
- To elucidate the mechanisms behind improved coronary flow reserve in hypertensive patients.
Main Methods:
- Studies in spontaneously hypertensive rats (SHRs) treated with various antihypertensive drugs (hydralazine, felodipine, lisinopril, nifedipine, moxonidine).
- Assessment of left ventricular hypertrophy (LVH), myocardial fibrosis, coronary vessel structure, and coronary flow reserve.
- Analysis of preliminary clinical data from hypertensive patients with microvascular disease undergoing prolonged antihypertensive treatment.
Main Results:
- Hydralazine enhanced coronary reserve in SHRs without LVH regression.
- Felodipine reversed medial hypertrophy in coronary resistance vessels.
- Lisinopril improved coronary reserve and reversed medial hypertrophy and myocardial fibrosis in SHRs.
- Nifedipine and moxonidine increased capillary length density in experimental hypertension.
- Clinical data suggest improved coronary flow reserve in hypertensive patients after treatment.
Conclusions:
- Antihypertensive therapy can potentially reverse cardiac remodeling and improve coronary microcirculation.
- Further studies are required to differentiate the effects of myocardial factors versus microcirculatory repair on coronary flow reserve.
- Understanding these mechanisms is crucial for optimizing treatment strategies for hypertensive cardiac complications.
Abstract:
In arterial hypertension, cardiac remodeling comprises myocyte hypertrophy, interstitial fibrosis, and functional and structural alterations of the coronary microcirculation. This leads to diastolic and systolic dysfunction of the left ventricle and impairment of coronary flow reserve. Consequently, antihypertensive treatment should aim at repairing hypertensive cardiac remodeling through reversing myocyte hypertrophy, restoring myocardial structure, and improving coronary flow reserve along with blood pressure normalization. Although it has been shown that regression of left ventricular hypertrophy (LVH) can be achieved by suitable antihypertensive therapy, more insight regarding the ability to repair coronary microcirculation is needed. In spontaneously hypertensive rats (SHRs), it has been shown that coronary reserve was enhanced after hydralazine administration without concomitant regression of LVH. Likewise, administration of the calcium-channel blocker felodipine led to a reversal of medial hypertrophy in coronary resistance vessels. The angiotensin-converting enzyme inhibitor lisinopril was shown to improve coronary reserve and to reserve both medial hypertrophy and myocardial fibrosis in SHRs. Increase in length density of capillaries with either nifedipine or moxonidine treatment was also found in experimental hypertension. First clinical data indicate that, after prolonged antihypertensive treatment, coronary flow reserve can be improved in hypertensive patients with microvascular disease. Further studies are warranted to elucidate whether improved coronary flow reserve after medical treatment for arterial hypertension is due to an influence of myocardial factors, such as LVH or myocardial fibrosis or to repair of the structurally remodeled microcirculation.