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Published on: February 3, 2021
Management of the hypertensive patient with coronary insufficiency but without atherosclerosis
Michael Preik1, Malte Kelm, Bodo-Eckehard Strauer
1Universitätsklinikum Düsseldorf, Medizinische Klinik und Poliklinik B, Klinik für Kardiologie, Pneumologie, Angiologie, Düsseldorf.
Insights
Hypertension causes coronary microvascular disease, leading to angina without artery blockages. Restoring microvascular function is key for managing hypertensive heart issues and preventing cardiac events.
Area of Science:
- Cardiology
- Hypertension Research
- Vascular Biology
Background:
- Arterial hypertension is a significant risk factor for angina pectoris with normal coronary arteries.
- Structural and functional abnormalities in coronary circulation, including extravascular factors like left-ventricular hypertrophy, impair coronary blood flow relative to oxygen demand.
- Hypertensive microvascular disease involves functional disturbances and morphologic changes in the coronary microvasculature, reducing coronary conductance.
Purpose of the Study:
- To highlight the importance of functional disturbances in the coronary microvasculature of hypertensive patients.
- To discuss diagnostic approaches for hypertensive microvascular disease.
- To emphasize the therapeutic goal of restoring coronary microvascular integrity in hypertensive patients without atherosclerosis.
Main Methods:
- Qualitative assessment using Doppler echocardiography and stress tests for noninvasive monitoring.
- Invasive procedures for quantitative assessment.
- Review of current therapeutic strategies targeting the renin-aldosterone-angiotensin-II system.
Main Results:
- Hypertensive microvascular disease can be diagnosed noninvasively and monitored.
- Restoration of microvascular function is a critical therapeutic target.
- Reversal of factors like left-ventricular hypertrophy and diastolic dysfunction is crucial.
Conclusions:
- Hypertensive microvascular disease contributes to angina and cardiac events in patients without epicardial coronary stenosis.
- Noninvasive and invasive methods aid in assessing coronary microvascular function.
- Targeting the renin-aldosterone-angiotensin-II system with ACE inhibitors, ARBs, and aldosterone antagonists shows promise for improving coronary insufficiency in hypertensive patients.
Abstract:
Arterial hypertension is a major risk factor for the clinical syndrome of angina pectoris, in which the ECG is abnormal but the coronary arteries are normal. Structural and functional abnormalities in coronary circulation as well as extravascular factors (eg, left-ventricular hypertrophy, fibrosis with diastolic dysfunction) compromise the adequate ratio of coronary blood flow to oxygen demand causing angina, dyspnea, and major cardiac events. Recent studies stress the importance to functional disturbances of coronary microvasculature leading to profound morphologic changes associated with impaired coronary conductance. In patients without epicardial coronary stenosis hypertensive microvascular disease can be qualitatively assessed by noninvasive diagnostic approaches based on new Doppler echocardiography techniques and may also be monitored by widely available stress tests. For ultimate quantitative assessment, invasive procedures are still required. Beyond guidelines to control blood pressure in hypertensive individuals, restoration of functional and structural integrity of the coronary microvasculature represents the ultimate therapeutic goal in hypertensive patients with coronary insufficiency and without angiographic evidence of atherosclerosis. Concomitant factors reducing coronary conductance such as left-ventricular hypertrophy and diastolic dysfunction should be reversed in parallel. Currently, therapeutic intervention in the renin-aldosterone-angiotensin-II-system using ACE inhibitors, angiotensin receptor blockers, and low doses of aldosterone antagonists represent the most promising strategy to achieve these goals. Using the knowledge of these recent results we should refine the overall management of our hypertensive patients with coronary insufficiency but without atherosclerosis.
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