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Correlation between the exercise-induced increase in left ventricular filling pressure and the extent of ischemic or
1First Department of Internal Medicine, Nagoya University School of Medicine, Japan.
Insights
Left ventricular filling pressure correlates with exercise-induced ischemia in angina patients. However, old myocardial infarction patients show no such correlation, suggesting different compensatory mechanisms possibly influenced by ventricular remodeling.
Area of Science:
- Cardiology
- Cardiovascular Physiology
Background:
- Coronary artery disease (CAD) involves impaired myocardial perfusion.
- Left ventricular filling pressure (LVFP) is a key indicator of cardiac function.
- The relationship between LVFP and myocardial damage extent in CAD requires further elucidation.
Purpose of the Study:
- To investigate the correlation between LVFP and the extent of ischemic or infarcted myocardium in patients with CAD.
- To differentiate compensatory mechanisms in transient ischemia versus old myocardial infarction.
Main Methods:
- Studied 39 patients with CAD (25 angina, 14 old myocardial infarction).
- Measured hemodynamic parameters at rest and during exercise.
- Assessed myocardial ischemia/infarct extent and severity using thallium-201 (201Tl) SPECT.
Main Results:
- In angina patients, ischemia extent/severity strongly correlated with peak exercise pulmonary artery wedge pressure (PAWP).
- In old myocardial infarction patients, infarct extent/severity correlated with left ventricular ejection fraction (LVEF) but not PAWP.
- No correlation found between infarct extent and LVFP in old myocardial infarction patients.
Conclusions:
- Dynamic exercise elicits different compensatory mechanisms in transient ischemia versus old infarction.
- Ventricular remodeling may influence compensatory mechanisms in patients with old myocardial infarction.
- LVFP is a relevant hemodynamic parameter for assessing exercise-induced ischemia in angina but not old infarcts.
Abstract:
We investigated the correlation between left ventricular filling pressure and the extent of ischemic or infarcted myocardium in 39 patients with coronary artery disease: 25 with angina pectoris (group A) and 14 with old myocardial infarction but without overt transient myocardial ischemia (group B). Hemodynamic parameters were measured at rest and during exercise. The extent and severity scores of ischemia or infarct were calculated using thallium-201 (201Tl) myocardial single-photon emission computed tomography. In group A, the extent and severity scores of ischemia were strongly correlated with pulmonary artery wedge pressure at peak exercise (r = 0.71, p < 0.001, r = 0.62, p < 0.01, respectively). In group B, the extent and severity scores of the infarct were significantly correlated with left ventricular ejection fraction (r = -0.81, p < 0.001, r = -0.77, p < 0.01, respectively), but were not correlated with pulmonary artery wedge pressure. Since no relationship was found between the extent of infarct and left ventricular filling pressure, dynamic exercise appears to elicit a different compensatory mechanisms in nonischemic myocardium for exercise-induced transient ischemia and in noninfarcted myocardium for old infarction. The compensatory mechanism in patients with old myocardial infarction may be affected by ventricular remodeling.