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Systolic ventricular dysfunction and heart failure due to coronary microangiopathy in hypertensive heart disease
1Medical Clinic, Heinrich-Hèine-University of Düsseldorf, Germany.
Insights
Arterial hypertension causes left ventricular hypertrophy through myocyte changes and fibrosis, impairing coronary blood flow. Antihypertensive treatment can reverse these effects, aiding cardiac function and preventing heart failure.
Area of Science:
- Cardiology
- Hypertension Research
- Cardiac Physiology
Background:
- Arterial hypertension is a leading cause of left ventricular hypertrophy (LVH).
- LVH involves myocyte and interstitial changes, alongside intramural coronary artery alterations.
- Hypertensives exhibit reduced coronary vasodilator reserve due to microcirculation dysfunction.
Purpose of the Study:
- To elucidate the mechanisms linking arterial hypertension, LVH, and impaired cardiac function.
- To investigate the role of coronary microcirculation in hypertensive heart disease.
- To assess the potential for reversing hypertensive cardiac pathology with treatment.
Main Methods:
- This study reviews the structural and functional alterations in the hypertensive heart.
- It examines the impact of impaired coronary vasodilator reserve on myocardial perfusion.
- The analysis considers the interplay between structural changes and functional outcomes.
Main Results:
- Hypertension-induced LVH is characterized by myocyte hypertrophy, fibrosis, and coronary artery structural changes.
- Reduced coronary vasodilator reserve in hypertensives leads to malperfusion and malnutrition.
- Increased diastolic filling pressure exacerbates coronary resistance.
- These factors collectively result in depressed myocardial performance and contractile dysfunction.
Conclusions:
- Structural alterations in the myocardium, interstitium, and coronary vasculature initiate and sustain myocardial malperfusion and malnutrition.
- This process leads to functional depression, loss of contractile proteins, and decreased contractile function in long-standing LVH.
- Effective antihypertensive treatment can reverse these pathological processes, potentially renormalizing cardiac function and preventing heart failure.
Abstract:
Left ventricular hypertrophy in arterial hypertension is characterized by myocyte hypertrophy, myocardial fibrosis, and structural changes of the intramural coronary arteries. Hypertensives with or without left ventricular hypertrophy have a reduced coronary vasodilator reserve due to alterations of the coronary microcirculation. The impairment in coronary vasodilator reserve is likely to initiate a process of malperfusion and malnutrition concomitant with increased metabolic demands. Further, malperfusion is supported by an increase in diastolic filling pressure, which will enhance the extravascular component of coronary resistance. The sum of interactions of these structural alterations of myocardium, interstitium, and coronary vasculature are likely to initiate and maintain a process of myocardial malperfusion and malnutrition, which can provoke functional depression of the myocardial performance, a loss of contractile proteins, an increase in interstitial fibrosis, and, not least, an overall decrease in contractile function in long-standing cardiac hypertrophy. Finally, the reversal of these processes by adequate antihypertensive treatment may contribute to renormalization of cardiac function and to prevention of late cardiac failure in hypertensive heart disease.