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Left ventricular circumferential wall stress at end-diastole (preload) and at the end of isovolumic left ventricular contraction (afterload) was calculated in 48 subjects with chronic myocardial and valvular heart disease by using left ventricular internal dimensions and wall thickness measured by quantitative echocardiography, left ventricular end-diastolic pressure, and aortic end-diastolic pressure. These calculations were then compared with similar determinations made using quantitative angiocardiography. Left ventricular preload and afterload determined by quantitative echocardiography and quantitative angiocardiography correlated significantly (r = 0.978 and 0.864, respectively). Left ventricular preloads of 30 X 10 3 dynes/cm 2 in subjects with mitral stenosis and 39 X 10 3 dynes/cm 2 in subjects with coronary artery disease unassociated with left ventricular dysfunction or mitral regurgitation were close to or within the normal range (32 X 10 3 ± 4 X 10 3 dynes/cm 2 ). Left ventricular preload in subjects with compensated volume overload was comparable with the angiocardiographically calculated values of 63 x 10 3 , 57 X 10 3 , and 53 X 10 3 dynes/cm 2 in subjects with coronary artery disease plus mitral regurgitation, mitral regurgitation, and aortic regurgitation, respectively. Left ventricular preload was most elevated in subjects with coronary artery disease associated with segmental left ventricular dyskinesis or akinesis. No significant differences in left ventricular afterload were noted between subject groups, although those with hypertrophic cardiac disease had the lowest calculated values. Quantitative echocardiography is an accurate technique for measuring left ventricular circumferential wall stress (preload and afterload) when left ventricular end-diastolic pressure and aortic end-diastolic pressure can be obtained. KEY WORDScircumferential wall stress ultrasound left ventricular geometry left ventricular hypertrophy left ventricular wall thickness valvular heart disease coronary artery disease • The adaptive anatomic and functional alterations of the left ventricle produced by chronic myocardial or valvular heart disease c an be evaluated by measuring ventricular volume, intracavitary pressure, and mass. Quantitative angiocardiography (1) has facilitated description of the mechanical function of the ventricle in the normal state (2) and in a variety of abnormal conditions (3, 4). However, evaluation of ven-

Twenty-two patients with shock complicating myocardial infarction were studied hemodynamically and, despite pharmacologic therapy and regulation of intravascular volume, 16 (73%) subsequently expired. Pulmonary artery end-diastolic pressure (PAEDP) or left ventricular end-diastolic pressure (LVEDP) was > 15 mm Hg in 18 of the 22 patients, and cardiac index (CI) was <2.3 liters/min/m2 in 17 of 22 patients. Fourteen of the 18 patients with PAEDP or LVEDP > 15 mm Hg expired, while two of the four patients with a PAEDP or LVEDP < 15 mm Hg survived. Thirteen of 15 individuals with a CI < 2.3 liters/min/m2 died, and four of seven with a CI > 2.3 liters/min/m2 survived. A ventricular gallop (S.) was audible in 15 patients with PAEDP or LVEDP varying from 13 to 60 mm Hg. In 11 patients with an S, who expired, the PAEDP or LVEDP ranged from 22 to 60 mm Hg. Mean peripheral vascular resistance was 41.3 units in survivors and 67.8 units in nonsurvivors. Six of eight patients who did not survive the period of hospitalization had a depressed response to dextran infusion manifested by a greater increase in PAEDP or LVEDP than in CI.Hemodynamic evaluation permitted early identification of measurements associated with 100% mortality despite intensive medical treatment. These findings included: (1) PAEDP or LVEDP > 28 mm Hg and (2) PAEDP or LVEDP > 15 mm Hg in association with a CI < 2.3 liters/min/m2. Patients in cardiogenic shock with these hemodynamic alterations are presumably candidates for cardiocirculatory mechanical assisting devices and possibly for further surgical intervention. Additional Indexing Words: Dextran infusion Digoxin ] Isoproterenol Norepinephrine Prog W ITH the development of intensive coronary care units and continuous electrocardiographic monitoring, significant

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