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Effects of a meal on hemodynamic function at rest and during exercise in patients with hypertrophic cardiomyopathy
D M Gilligan1, W L Chan, E L Ang
1Division of Clinical Cardiology, Royal Postgraduate Medical School, Hammersmith Hospital, London, England.
Insights
Eating can worsen hypertrophic cardiomyopathy symptoms. A meal caused abnormal blood flow changes, including increased heart pressures and reduced stroke volume, especially during exercise, potentially leading to collapse.
Area of Science:
- Cardiology
- Physiology
Background:
- Hypertrophic cardiomyopathy (HCM) patients often report symptom worsening after meals.
- Post-meal vasodilation may negatively impact HCM, particularly during exertion.
Purpose of the Study:
- To investigate the hemodynamic effects of a meal on patients with hypertrophic cardiomyopathy during rest and exercise.
Main Methods:
- 11 HCM patients underwent invasive hemodynamic monitoring.
- Exercise testing was performed in both fasting and postprandial (45 min after a 740 kcal meal) states.
Main Results:
- A meal decreased systemic vascular resistance and increased right atrial, pulmonary artery, and pulmonary capillary wedge pressures.
- Postprandial exercise showed higher heart rate, cardiac index, and filling pressures compared to fasting exercise.
- Patients with pre-existing postprandial symptom exacerbation exhibited a blunted increase in stroke volume and cardiac index.
Conclusions:
- Patients with HCM demonstrate an abnormal hemodynamic response to food intake.
- This response includes a failure of stroke volume to increase and elevations in pulmonary pressures.
- These adverse hemodynamic changes during postprandial exercise may increase the risk of exertional collapse in some HCM patients.
Abstract:
Many patients with hypertrophic cardiomyopathy experience postprandial exacerbation of their symptoms. The vasodilation associated with eating may be deleterious in hypertrophic cardiomyopathy, especially during exercise. To examine the hemodynamic effects of a meal in hypertrophic cardiomyopathy, 11 patients were studied with invasive hemodynamic monitoring during exercise testing in the fasting state and 45 min after a 740 kcal (3,100 J) meal. The meal induced a decrease in systemic vascular resistance index at rest (mean +/- SD, -17 +/- 14%), increases in mean right atrial (31 +/- 21%), mean pulmonary artery (14 +/- 14%) and mean pulmonary capillary wedge (17 +/- 14%) pressures and an increase in cardiac index (18 +/- 10%) due to an increased heart rate without any significant change in stroke volume. During postprandial exercise, heart rate, rate-pressure product, cardiac index and cardiac filling pressures were higher than during fasting exercise and one patient had a decrease in exercise blood pressure compared with the fasting test. Five patients with postprandial exacerbation of symptoms in everyday life had a lesser increase in systemic arterial pressure and stroke volume during both exercise tests and a smaller increase in cardiac index after the meal than did the six patients without postprandial symptom exacerbation, suggesting more severe cardiac disease. It is concluded that patients with hypertrophic cardiomyopathy have an abnormal hemodynamic response to food, in which stroke volume fails to increase and pulmonary capillary wedge and pulmonary artery pressures increase. These adverse changes persist during postprandial exercise and may predispose to exertional collapse in certain patients.