Rise In Left Ventricular End-diastolic Pressure Research Articles

Left ventricular hemodynamics in patients with coronary artery disease and in normal subjects: Correlations with the extent of coronary artery lesions and the electrocardiogram

Left ventricular hemodynamics were studied during supine leg exercise immediately prior to coronary arteriography in seventy-one patients with coronary artery disease and nineteen without evidence of heart disease. Patients were divided into six groups, based on the number of major coronary arteries (right coronary, left anterior descending, left anterior descending diagonal, left circumflex, left circumflex marginal) with greater than 75 per cent obstruction. Mean resting and exercise left ventricular end-diastolic pressure (LVEDP) and increase in LVEDP during supine exercise rose progressively with more extensive coronary artery disease. All patients without coronary artery disease or with disease confined to one coronary artery had LVEDP of less than 24 mm Hg during exercise. There was no significant difference between groups with coronary artery disease in regard to stroke volume, heart rate and systemic arterial pressure. There was no significant difference in LVEDP at rest or during exercise between patients with normal and those with abnormal resting electrocardiograms. However, in patients with abnormal electrocardiograms after exercise, the mean LVEDP was significantly higher than in those with normal electrocardiograms after exercise (P < 0.05). Other hemodynamic differences between patients with normal and those with abnormal electrocardiograms after exercise were insignificant. The degree of rise in LVEDP with supine leg exercise in patients who have coronary artery disease is in part related to the number of coronary arteries with severe obstruction, and an abnormal electrocardiogram after exercise is associated with a high LVEDP during exercise.

A reproducible model of cardiogenic shock in the dog.

An animal model of cardiogenic shock has been developed in the intact unanesthetized dog. Selective embolization of the circumflex coronary artery with 0.2 ml of mercury produces infarction of the posterolateral wall of the left ventricle and a shocklike state in the dog which results in death of the animal in 5 to 48 hr. The syndrome of cardiogenic shock in the animal model simulates closely that observed in man. Systemic blood pressure falls sharply (25 to 30% of control) immediately after embolization, remains low for several hours, then slowly increases toward normal, but never reaches preinfarct levels. The left ventricular end-diastolic pressure (LVEDP) remains within normal limits (5 to 10 mm Hg) during the initial hypotensive state, but increases to values above 10 mm Hg during the period of rising systemic pressures. As left ventricular failure begins to develop as evidenced by the rise in LVEDP, the mean pulmonary artery pressure also rises above control values. The cardiac output falls to 40% of control levels following embolization and never recovers. Peripheral resistance rises to compensate for the reduction of cardiac output and remains above control levels. Electrocardiograms indicate an essentially normal sinus rhythm with short runs (5 to 15 beats) of ventricular tachycardia with A-V dissociation. The hypotensive state does not seem to be related to this arrhythmia. Death of the animal appears to be due to progressive failure of the left ventricular pump to maintain cardiac output and systemic pressures.

Left ventricular performance during mild supine leg exercise in coronary artery disease.

Left ventricular (LV) performance was studied during mild exercise (100 kg-m/min for 3 minutes) in 19 cases of coronary artery disease (CAD). Each patient suffered from a severe anginal syndrome. None had ventricular aneurysm, cardiomegaly, or clinical heart failure. Mean resting values follow: LV end-diastolic pressure (LVEDP), 19 ± 7 mm Hg; LV systolic pressure (LVSP), 150 ± 16 mm Hg; stroke volume index (SVI), 48 ± 10 ml/beat/m 2 ; and LV stroke work index (LVSWI), 81 ± 19 g-m/m 2 . During exercise LVEDP rose to 30 ± 8 mm Hg ( P ≤0.001) and LVS to 160 ± 20 (not significant [NS]); SVI diminished to 46 ± 11 (NS) and LVSWI, to 76 ± 24 (NS). Patients with decreased or asynchronous areas of LV myocardium identified on cine left ventriculograms had higher mean LVEDPs during exercise than did those with normal ventriculograms (34 ± 10 versus 26 ± 4 mm Hg; P ≤0.05). The difference between responses to exercise of patients who experienced angina during the study and of those who did not was NS. Administration of nitroglycerin reduced the increase in LVEDP during exercise. An abnormality in LV performance-a significant rise in LVEDP without a significant increase in SVI or LVSWI-was observed in 13 of 19 cases of CAD.