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[Hemodynamic study in hypertensive cardiopathy under ischemia induced by atrial stimulation in the absence of fixed
Insights
Myocardial ischemia in hypertensive heart disease patients does not significantly alter left ventricular pressures during atrial pacing. Recovery shows a marked rise in left ventricular end-diastolic pressure, suggesting a depressed Starling curve mechanism.
Area of Science:
- Cardiology
- Cardiovascular Physiology
- Hypertension Research
Context:
- Hypertensive heart disease (HHD) presents unique challenges in understanding myocardial ischemia.
- Patients with HHD often exhibit left ventricular hypertrophy and resting ST-segment depression.
- Normal coronary arteries in HHD patients with ischemia suggest non-obstructive causes.
Purpose:
- To investigate hemodynamic changes during induced myocardial ischemia in HHD patients.
- To determine the role of left ventricular systolic pressure (LVSP) and left ventricular end-diastolic pressure (LVEDP) in ST-segment depression.
- To compare the functional impact of ischemia in HHD with obstructive coronary artery disease.
Summary:
- Atrial pacing (AP) induced myocardial ischemia in 7 HHD patients with normal coronary arteries.
- LVSP remained unchanged, while LVEDP showed a statistically significant but not hemodynamically critical rise during AP.
- LVEDP markedly increased upon cessation of AP, indicating a depressed Starling curve mechanism similar to obstructive coronary disease.
Impact:
- Neither LVSP nor LVEDP are primary drivers of ST-segment depression in this HHD cohort.
- The functional significance of ischemia in HHD may be similar to obstructive coronary disease, despite different pathogenetic mechanisms.
- Findings contribute to understanding the pathophysiology of ischemia in HHD and its management.
Abstract:
With the purpose to study the haemodynamic changes that occur with myocardial ischaemia induced by atrial pacing (AP) in hypertensive heart disease, we studied 7 patients with such condition, all of them with a long time history of systemic hypertension, electrocardiographic signs at rest of left ventricular hypertrophy and ST-segment depression, at least of 0.5 mm. All the patients showed normal coronary arteries in angiocardiogram. AP was started 10 beats above the basal heart rate with increments of 10 beats every 2 minutes until a ST-segment depression at least of 2 mm was obtained which occurred in all the cases studied. After every 2 minutes of AP a simultaneous 12-leads electrocardiogram recording and left ventricular and aortic pull-back pressure were obtained. At the desired end point the AP was abruptly stopped and the same parameters were registered at 3, 5, 10 and 15 minutes until recovery. During AP the left ventricular systolic pressure (LVSP) did not show any significant change, with the exception of a patient who experienced angor pectoris during the proceeding. The left ventricular end-diastolic pressure (LVEDP) increased in 3.4 +/- 1.7 mmHg, change that was statistically significant (p less than or equal to 0.01) but not hemodynamically important since only in one patient it increased above the normal levels (from 13 mmHg basal to 17 mmHg during AP). In contrast, LVEDP markedly rose above normal when AP was stopped. It is concluded that neither LVEDP nor LVSP play an important role in the genesis of the ST segment depression seen in these patients. It is showed that, similar as in patients with obstructive coronariopathy, these cases work on a depressed Starling curve during AP and its recovery for what is thought that the functional meaning of ischaemia for both entities is similar no matter that their pathogenetic mechanisms are different.