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Changes in diastolic properties of the regional myocardium during pacing-induced ischemia in human subjects
Insights
During angina, left ventricular diastolic pressure significantly increases, impacting diastolic properties and reducing ejection fraction. Impaired diastolic function in ischemic segments contrasts with preserved function in normal segments during stress.
Area of Science:
- Cardiology
- Cardiovascular Physiology
Background:
- Coronary artery disease can affect left ventricular diastolic function.
- Understanding diastolic property alterations during angina is crucial for patient management.
Purpose of the Study:
- To investigate the mechanisms of altered left ventricular diastolic properties during angina.
- To assess the impact of pacing-induced angina on diastolic function and myocardial mechanics.
Main Methods:
- Studied seven patients with coronary artery disease undergoing cardiac pacing.
- Utilized single-plane left ventriculography and micromanometer-tipped catheters.
- Analyzed diastolic pressure-volume relationships and regional myocardial function.
Main Results:
- Pacing-induced angina increased left ventricular end-diastolic pressure (p < 0.005) and reduced ejection fraction (p < 0.05).
- Diastolic pressure-volume curves shifted upward or rightward post-pacing.
- Normal segments showed increased end-diastolic length and stroke excursion, while ischemic segments had unchanged length and reduced shortening.
Conclusions:
- Angina significantly impairs left ventricular diastolic properties, independent of end-diastolic volume changes.
- Ischemic myocardial segments exhibit reduced function and altered diastolic mechanics during stress.
- These findings highlight the detrimental effects of ischemia on diastolic function in coronary artery disease.
Abstract:
Mechanisms related to alterations in the diastolic properties of the left ventricle during angina were studied in seven patients with coronary artery disease. Single plane left ventriculograms were obtained using a high fidelity micromanometer-tipped catheter in both the resting state and immediately after rapid cardiac pacing. In all patients, typical anginal pain developed with pacing stress. After atrial pacing, the left ventricular end-diastolic pressure increased from 10 +/- 3 to 21 +/- 7 mm Hg (+/- standard deviation) (p less than 0.005) regardless of the changes in the end-diastolic volume. The ejection fraction was reduced from 59 +/- 10 to 48 +/- 13% (p less than 0.05). The diastolic pressure-volume curves shifted upward in post-pacing beats in four patients, while in three the curves shifted more to the right. The regional myocardial function was expressed in quantitative terms by a radial coordinate system with the origin at the center of gravity of the end-diastolic silhouette. Two representative radial grids for normal and ischemic segments were selected. In the normal segment, the end-diastolic length was augmented by 15% (p less than 0.005) and was associated with a 24% increase in stroke excursion with pacing stress (p less than 0.05). The increase in diastolic pressure was accompanied by comparable increases in end-diastolic length, and the diastolic pressure-length relation moved up to the higher portion of the single curve. In the ischemic segment, the end-diastolic length remained unchanged in the post-pacing beat, but segment shortening was significantly reduced.(ABSTRACT TRUNCATED AT 250 WORDS)