Acute cardiogenic pulmonary edema: Relevance of multivessel disease, conduction abnormalities and silent ischemia

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Abstract

The frequency distribution and severity of the cardiac disease underlying acute cardiogenic pulmonary edema (APE) to define appropriate subsequent diagnostic and management strategies were investigated in 216 consecutive patients. To this effect, the clinical, electrocardiographic, ecocardiographic and angiographic characteristics were analyzed. Coronary artery disease was identified in 185 patients (86%)—146 with acute myocardial infarction—as the underlying cause, isolated valvular disease in 10 (5%) and other causes in 21 (11%). Most patients were elderly (≥70 years, 72%), hypertensive (71%) and diabetic (44%). Among coronary disease (CAD) patients, however, 105 (57%) showed conduction disturbances in the ECG (QRS>0.10 s) and 84 (45%) had no anginal pain during pulmonary edema. A 2D echocardiogram showed a 30% incidence of moderate–severe mitral regurgitation in coronary disease and non-coronary disease patients, and a 67% incidence of reduced ejection fraction (<50%), particularly in coronary disease patients (73%). A coronary angiography performed in 99 patients with coronary disease showed multivessel disease in 89 (91%) with a 32% incidence of significant left main disease.

Therefore, these findings demonstrate that coronary disease is the most common cause of acute pulmonary edema and it is associated with a distinctly high prevalence of multivessel and left main disease. This diagnosis, however, may often be overlooked if no serial enzymatic sampling is performed given the increased frequency of conduction abnormalities and lack of anginal pain.

Introduction

Acute cardiogenic pulmonary edema (APE) is a severe cardiac complication which may often be fatal if unattended and that may be caused by a variety of cardiac diseases, including coronary disease (CAD). Although in patients with chronic heart failure, there appears to be a preponderance of CAD [1], [2], [3], [4], in those with APE the distribution of the different causes remains ill defined for it has not been prospectively investigated. This is of importance for even though acute management is similar in different cardiac diseases, subsequent diagnostic and therapeutic strategies may differ significantly. On the other hand, since APE tends to be a complication of the elderly [5], [6], [7], [8], one may be tempted to avoid diagnostic invasive procedures if no clear clinical grounds point to a specific pathology. Therefore, the purpose of the study was to prospectively identify the underlying cardiac disease in consecutive patients with APE admitted to a tertiary center by performing a 12-lead ECG, determinations of markers of myocardial necrosis, a 2D echocardiogram and a coronary angiography.

Section snippets

Patients

A total of 216 consecutive patients admitted to our emergency room with APE between February 2000 and December 2001 were prospectively included. APE was defined by the presence of orthopnea of sudden onset (≤6 h), inspiratory rales, documented hypoxemia (arterial oxygen saturation <90%, with or without oxygen supply) and alveolar and/or interstitial pulmonary edema at the chest X-ray. Patients with chronic heart failure who presented progressive aggravation of their pulmonary congestion were

Underlying heart disease

Of the 216 patients, 185 (86%) were diagnosed of CAD of whom 146 (79%) had an acute myocardial infarction and 19 had an associated aortic stenosis (10%). Of the remaining 31, 10 (32%) presented valvular heart disease, 13 (42%) hypertensive cardiomyopathy, 1 (3%) a dilated cardiomyopathy, and 7 (23%) had apparently no cardiac disease although 3 of them had chronic atrial fibrillation. A coronary angiography was performed in seven patients with valvular disease and in three with hypertensive

Discussion

The main findings of this prospective study were that CAD, severe in most instances, was the most common cardiac disease underlying APE and that it was frequently associated with silent myocardial ischemia or infarction and/or ventricular conduction abnormalities. Moreover, APE developed mostly in elderly patients with a high incidence of hypertension and diabetes mellitus, and a rather high rate of generalized arteriosclerosis.

Limitations

Although this was a prospective study, it was not possible to perform a coronary angiography in all patients. Hence, there is a possibility that the predominant pattern of extensive disease could mainly reflect a biased selection of the sicker patients for angiography. However, those patients in whom angiography was not carried out were older and presented more frequent serious comorbidity factors and hence were likely to be at a higher risk for events and to show an extent of coronary disease

Implications

An important practical implication of our findings is the remarkably high incidence of CAD among consecutive patients with APE admitted to a tertiary center. They also underscore the diagnostic value of sequential measurements of necrosis markers for these patients frequently present without anginal pain and with conduction abnormalities in the electrocardiogram that may preclude suspicion of CAD. Moreover, recognition of the high frequency of multivessel disease needs also to be taken into

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