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Ultrasound Based Assessment of Coronary Artery Flow and Coronary Flow Reserve Using the Pressure Overload Model in Mice
Published on: April 13, 2015
[The flow-pressure relationship in coronary perfusion in myocardial hypertrophy in hypertension]
N De Cesare1, A Apostolo, F Fabbiocchi
1Istituto di Cardiologia, Università degli Studi, Milano.
Insights
Hypertension with cardiac hypertrophy reduces coronary flow reserve. In severe cases, coronary blood flow may decline even with normal perfusion pressure, indicating compromised myocardial oxygen supply.
Area of Science:
- Cardiovascular Physiology
- Coronary Circulation
- Hemodynamics
Context:
- Coronary flow reserve is crucial for myocardial oxygen supply.
- Hypertension and cardiac hypertrophy can alter coronary autoregulation and vasodilation.
- Understanding these changes is vital for diagnosing and managing cardiac conditions.
Purpose:
- To investigate the impact of hypertension and cardiac hypertrophy on coronary flow reserve.
- To determine if reduced flow reserve leads to decreased coronary blood flow at normal perfusion pressures.
Summary:
- This study examined coronary blood flow in normotensive and hypertensive individuals with varying degrees of cardiac hypertrophy.
- Coronary perfusion pressure was reduced, and flow reserve was assessed using thermodilution.
- Patients with significant left ventricular hypertrophy showed a decline in coronary blood flow and increased myocardial oxygen extraction at lower perfusion pressures.
Impact:
- Findings suggest that severe cardiac hypertrophy in hypertensive patients compromises coronary flow reserve.
- This can lead to reduced myocardial blood flow even at normal perfusion pressures, potentially increasing ischemia risk.
- Highlights the importance of assessing flow reserve in hypertensive patients with cardiac hypertrophy.
Abstract:
For any given perfusion pressure the difference between coronary autoregulated and maximally vasodilated flow represents the flow reserve. If hypertension and cardiac hypertrophy are present, the line of autoregulated flow becomes higher, and the pressure-flow relationship at maximal vasodilation less steep, due to the raised resistance. In these circumstances, flow reserve reduces and the point at which rest flow equals maximal achievable flow may be shifted to a higher perfusion pressure. Thus, flow would decline even if the perfusion pressure is lowered to normal. We tested this point in a setting of patients having chest pain and normal angiography of the left epicardial branches. Baseline flow (ml/min) from the great cardiac vein (thermodilution) was 142 +/- 13 in 9 normotensives (controls), 144 +/- 15 in 7 hypertensives (Group 1) with normal (114 +/- 11 g) left ventricular mass index and 188 +/- 17 in 8 hypertensives (Group 2) whose left ventricular mass (171 +/- 24 g) exceeded the mean +2 SD of normal. Coronary perfusion pressure was lowered in these patients by 5 mmHg every 5 minutes with a titrated nitroprusside infusion, taking as endpoints a perfusion pressure of 60 mmHg in the controls and of 70 mmHg in hypertensives. At endpoints, flow was similar to baseline in controls and Group 1. In Group 2 flow started to decline and myocardial oxygen extraction to slightly but significantly rise at perfusion pressure of from 90 to 80 mmHg; at the endpoint flow was reduced by 26% of baseline (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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