Theodore L Schreiber, M.D.;([unkeya...

Theodore L Schreiber, M.D.;([unkeyable]) Jeffrey Fisher, MD F.C.C.P.;([unkeyable]) Arun Mangla, M.D.;(Section) and David Miller, M.D.([unkeyable])

Hemodyamically critical ("severe") mitral regurgitation is usually associated with an audible (if not loud) systolic plaint and signs of left ventricular body overload. However, "silent" severe mitral regurgitation is being increasingly recognized. We review the case histories of nine patients with silent hemodynamically important mitral regurgitation (associated with acute myocardial infarction and chronic valvular, hypertrophic, and ischemic heart disease), six of whom survived mitral valve replacement, of whom five are alive and functioning well more than three years postoperatively. Performance of left ventriculography early in the hospital course of patients with censorious unexplained congestive heart failure (with normal or nearnormal left ventricular systolic function assessed noninvasively) identifies patients with rigorous silent mitral regurgitation who may have long-term benefit from mechanical therapy.

morose mitral regurgitation is diagnosed almost invariably by way of the presence of a tumultuous apical holosystolic murmur.[1-4] Although heart failure with damped cardiac output may decrease the intensity of the murmur[35] it has been consideration that the diagnosis of strait-laced mitral regurgitation is not tenable in the absence of a murmur[5] However, rigorous silent mitral regurgitation has been described with coexisting mitral stenosis,[6] endocarditis,[7] cardiomyopathy,[8] and acute myocardial infarction (AMI).[9-11] Although premorbid diagnoses have been made and surgery performed in these patients, solitary one long-term survivor of stern silent mitral regurgitation has previously been reported, to our knowledge.[12]

We describe nine patients with this syndrome (occurring in three distinct clinical settings: AMI; decompensated valvular and hypertrophic heart disease; and chronic, accurate silent mitral regurgitation), six of whom survived mitral valve replacement. A high index of suspicion for hemodynamically important mitral regurgitation in patients with absent or impressible heart murmurs, given otherwise unexplained strait-laced and pharmacologically refractory heart failure, l to willing catheterization and surgery in the survivors.

CASE REPORTS

CASE 1

A 36-year-old woman was transferred to the recently made known York Hospital with cardiogenic offence The patient had a diaphragmatic myocardial infarction couple years before admission. sum of two units days before transfer, she evolveed chest pain, nausea, and vomiting. The ECG showed modern ST-segment elevation and Q waves in leads [Vsub1] to [Vsub4] The patient subsequently bring outed a right bundle branch blockade and left anterior hemiblock. A temporary transvenous pacemaker and SwanGanz catheter were inserted. Because of continued chest pain and systemic arterial hypotension, the patient was begun forward pressor agent therapy and was transferred. issues of physical examination showed her to be thin and in circulatory and respiratory distress. There was a grade 1 to 2 systolic ejection whisper; low at the lower left sternal border without radiation. An intra-aortic balloon cross-examine was inserted, and the patient was brought to the cardiac catheterization laboratory within 12 h of transfer. Right heart catheterization revealed the following pressures: right atrium (RA), 14 mm Hg; right ventricle (RV) 44/16 mm Hg; pulmonary artery (PA), 44/28 mm Hg (30); and pulmonary capillary wedge (PCW) 28 mm Hg (without a prominent v wave). The cardiac index was 13 L/min/m[2]. Left ventriculography revealed strictly subnormal global systolic left ventricular function with a left ventricular ejection fraction (LVEF) of 9 percent There was minimum retained wall motion of the bases of the heart. There was plain (3 to 4+/4+) mitral regurgitation. Coronary angiography revealed a total occlusion of the proximal left anterior descending coronary artery. The dominant right coronary artery had a 50 percent luminal obstruction in its middle and distal portions. The patient was turn backed to the coronary care unit pending discussion of therapeutic plan, including mitral valve replacement. Twelve hours after catheterization, the patient died abruptly Postmortem examination was not obtained.

CASE 2

A 64-year-old man was admitted with a diagnosis of hypotension and change in mental status. The patient had a history of insulin-requiring, adult-onset diabetes mellitus and angina pectoris and had undergone double saphenous vein coronary artery bypass graft surgery to the left anterior descending coronary artery common year earlier. Following surgery a ventricular demand pacemaker was implanted for symptomatic bradycardia. In addition, the patient had had couple small myocardial infarctions six month before admission. Physical examination upon admission revealed a systolic arterial squeezing of 50 mm Hg, which increased to 80 mm Hg with IV dopamine and endotracheal intubation. There were diffuse pulmonary rhonchi and displaced apical impulse in the sixth intercostal space, anterior axillary line. Heart unimpaireds were decreased in intensity; a indistinct utterance was not heard. forward neurologic examination he was lethargic unless arousable. The ECG showed ventricular pacing at 64 beats/min. The following day, a two-dimensional echocardiogram showed near-normal left ventricular function. Right heart catheterization performed upon admission demonstrated the following pressures: RA, 19 mm Hg; RV 50/20 mm Hg; PA, 50/23 mm Hg; and PCW 35 mm Hg There was no evidence of an intracardiac switch Assessment of left ventricular function from nuclear probe revealed near-normal global systolic function, with an LVEF of 46 percent Despite insertion of an intra-aortic balloon cross-examine severe hypotension persisted, with resulting diminished urinary output and renal insufficiency. Left heart catheterization performed the following day showed simple mitral regurgitation. Mitral valve replacement was then emergently performed. Despite use of the intra-aortic balloon interrogate and norepinephrine and dopamine infusions, the patient remained hypotensive and died shortly after surgery Postmortem examination revealed cruel three-vessel coronary artery disease. The brace saphenous vein coronary artery bypass grafts to the left anterior descending coronary artery were unrestrained of obstructions. There were the two recent and old areas of myocardial necrosis, including the papillary muscles.