Cardiac Adaptation in Acute Hypertensive Pulmonary Edema

• Published in: The American journal of cardiology Vol. 109; no. 10; pp. 1472 - 1481
• Main Authors: Mǎrgulescu, Andrei D., MD, Rimbaş, Roxana C., MD, Florescu, Maria, MD, Dulgheru, Raluca E., MD, Cintezǎ, Mircea, MD, PhD, Vinereanu, Dragoş, MD, PhD
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 15.05.2012; Elsevier; Elsevier Limited
• Subjects: Acute Disease; Adaptation, Physiological; Aged; Arterial hypertension. Arterial hypotension; Biological and medical sciences; Blood and lymphatic vessels; Cardiac Volume - physiology; Cardiology. Vascular system; Cardiovascular; Cardiovascular disease; Echocardiography; Female; Heart; Heart failure, cardiogenic pulmonary edema, cardiac enlargement; Heart Ventricles - diagnostic imaging; Heart Ventricles - physiopathology; Humans; Hypertension - complications; Hypertension - diagnosis; Hypertension - physiopathology; Male; Medical sciences; Prognosis; Pulmonary Edema - diagnosis; Pulmonary Edema - etiology; Pulmonary Edema - physiopathology; Radiography; Studies; Ultrasonic imaging; Ventricular Dysfunction, Left - complications; Ventricular Dysfunction, Left - diagnosis; Ventricular Dysfunction, Left - physiopathology; Heart; Hypertension; Lung disease; Acute pulmonary edema; Respiratory disease; Cardiovascular disease; Circulatory system; Cardiology; Adaptation
• ISSN: 0002-9149; 1879-1913
• DOI: 10.1016/j.amjcard.2012.01.359

The aim of this study was to evaluate the role of left ventricular (LV) dysfunction (global and regional, systolic and diastolic) acute dyssynchrony, ischemic mitral regurgitation (MR), and afterload changes in acute hypertensive pulmonary edema (AHPE). Forty-four consecutive patients were evaluated by comprehensive echocardiography during clinical and radiologic pulmonary edema (63 ± 29 minutes after first dose of treatment) and after 48 to 92 hours. Twenty age- and gender-matched asymptomatic hypertensive and diabetic subjects served as controls. AHPE was associated with increased afterload (estimated arterial elastance 3.0 vs 2.3 mm Hg/ml, p = 0.024) and subsequent decreased longitudinal LV systolic function (mean strain of 6 basal segments −11.0% vs −15.4%; p = 0.015) compared to the stable follow-up state. However, global LV systolic function was maintained (estimated ventricular elastance 1.7 vs 1.6 mm Hg/ml, stroke work 76.7 vs 84.5 cJ, ejection fraction 0.33 vs 0.37, all nonsignificant). Except for diastolic filling time (ratio to cardiac cycle 0.41 vs 0.49, p <0.001), other indexes of diastolic function, dyssynchrony, and MR severity were similar between evaluations. Patients with AHPE had worse ventricular–arterial coupling, systolic function, estimated diastolic stiffness, and filling pressures compared to asymptomatic controls, suggesting a decreased capacity to adapt to changes in loading. In conclusion, acute alterations of systolic and diastolic LV function, myocardial synchrony, and ischemic MR are unlikely mechanisms of AHPE. Rather, AHPE is likely to develop in patients with decreased systolic and diastolic capacity to adapt to acute changes in loading.