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[The functional capacity of the coronary circulation in myocardial hypertrophy]
1Istituto di Cardiologia, Università degli Studi, Milano.
Insights
Hypertension with left ventricular hypertrophy impairs coronary blood flow regulation. This makes the heart vulnerable to low blood pressure, highlighting risks in clinical management.
Area of Science:
- Cardiology
- Physiology
- Hypertension Research
Background:
- Hypertensive hearts with left ventricular hypertrophy exhibit coronary circulation abnormalities.
- Clinical data suggest increased myocardial ischemia risk in these patients.
- Pathophysiology of coronary circulation in human hypertrophied hearts remains unclear.
Purpose of the Study:
- To investigate coronary flow regulation during reduced perfusion pressure in hypertensive patients with and without left ventricular hypertrophy.
- To determine the lower limit of coronary autoregulation in these patient groups.
Main Methods:
- Coronary flow was measured using thermodilution.
- Perfusion pressure was progressively reduced in hypertensive patients.
- Patients were stratified based on left ventricular mass.
Main Results:
- Coronary flow decreased at 90 mmHg in patients with myocardial hypertrophy.
- No significant coronary flow changes occurred until 70 mmHg in hypertensives without hypertrophy.
- Increased myocardial oxygen extraction was noted at 75 and 70 mmHg in hypertrophic hearts.
Conclusions:
- Coronary autoregulation shifts to higher perfusion pressure in hypertensive patients with left ventricular hypertrophy.
- The hypertrophied myocardium is vulnerable to relative hypotension.
- Clinical management should consider this altered autoregulation in hypertensive patients with hypertrophy.
Abstract:
Experimental studies showed anatomic and functional abnormalities in coronary circulation of hypertensive hypertrophic hearts. Epidemiologic and clinical data suggest that hypertensive patients with myocardial hypertrophy are more prone or sensitive to myocardial ischemia. Although several factors have been invoked to explain these observations, pathophysiological abnormalities in coronary circulation of hypertrophied hearts due to pressure overload in man are unsettled. Recently we evaluated coronary flow, through thermodilution, during progressive reduction of perfusion pressure in hypertensive patients with and without left ventricular hypertrophy. While in hypertensives with normal left ventricular mass, no significant changes of coronary flow were observed during reduction of perfusion pressure until 70 mmHg were reached, in patients with myocardial hypertrophy coronary flow began to decrease at 90 mmHg. Meanwhile, a small but significant increase of oxygen myocardial extraction was recorded at 75 and 70 mmHg. These data suggest that even in man when hypertension and hypertrophy are concomitant, the lower range of coronary autoregulation is shifted to a higher perfusion pressure and that under these conditions, the myocardium may be vulnerable to treatment-induced relative hypotension.