John D Rozich, MD; Jackie Kaiser RD...

John D Rozich, MD; Jackie Kaiser RDMS; and Douglas L Mann, MD

A 59-year-old man at handed with culture-negative endocarditis. Serial echocardiographic/Doppler studies disclosed progressive aortic insufficiency with resultant premature closure of the mitral valve. At the time the patient unfolded PMVC he was considered for emergent aortic valve replacement; ultimately, however, he was imagineed inoperable because of his underlying medical question s Surprisingly, the patient gradually improved forward antibiotic therapy alone, with posterior hemodynamic stabilization and reversion of the PMVC This case depicts the first description of reversion of PMVC in a medically treated patient with bitter aortic insufficiency secondary to infective endocarditis, and underscores the importance of basing management decisions concerning aortic valve replacement in infective endocarditis relating to the entire constellation of clinical findings rather than a single echocardiographic sign.

The increase of premature mitral value closure (PMVC) in patients with acute aortic insufficiency associated with infective endocarditis is generally regarded as an echocardiographic sign of rigid hemodynamic overload of the left ventricle. greatest in number studies[1-4] further suggest that patients who unravel PMVC in the setting of infective endocarditis be considered for emergent aortic valve replacement; indeed, the timing of aortic valve surgery may be based entirely on the subject of this echocardiographic sign.[4] This report discusses a unique case of a patient with culture-negative endocarditis who, despite having discloseed PMVC in the face of progressively simple aortic regurgitation, was managed medically, with resultant hemodynamic stabilization and reversion of the premature closure pattern of the mitral valve.

CASE REPORT

A 59-year-old man with a history of chronic obstructive pulmonary disease, cirrhosis, portal hypertension, esophageal varices and a chronic coagulopathy not absented to the emergency room with a three-week history of progressive dyspnea and a productive cough Physical examination disclosed an ill-appearing man in moderate respiratory distress, with a temperature of 383 [degrees] C offspring pressure of 160/60 mm Hg and a respiratory rate of 28/min. Examination of the lung disclosed bibasilar rales; auscultation of the heart revealed a grade 3/6 short midsystolic whisper; low along the left sternal border and a grade 2/6 diastolic complaint at the 2nd right intercostal space and along the left sternal border. The chest x-ray film showed a mildly enlarged cardiac silhouette with infiltrates involving the right lower and middle lobes and the left lower lobe; the admission electrocardiogram revealed sinus tachycardia with normal PR and QR intervals.

Hospital Course and Serial Echocardiographic Studies

cultivations were obtained and the patient started in succession intravenous antibiotics; in addition, the patient was started forward prazosin and furosemide (prn). in succession the second hospital day the patient lay opened acute respiratory failure and required mechanical ventilatory support. An echocardiographic/Doppler inquiry at that time showed a mildly dilated left ventricle (59 mm) with normal systolic function, a small pericardial effusion and minimal thickening of the non- and right coronary cusps of the aortic valve; the Q-C interval (ECG Q wave to mitral value closure point onward the M-mode echocardiogram) interval was normal at 007 s (Fig 1A). The pulsed-wave Doppler examination disclosed a diastolic be derived disturbance below the aortic valve leaflets with no evidence of a systolic liquefy disturbance in the left atrium.

Although the patient remained hemodynamically stable above the ensuing days, an echocardiographic/Doppler subject of attention on the 23rd hospital day showed progressive thickening of the aortic valve with the disentanglement of PMVC (Q-C=0.02 s [Fig 1B]) Given the progressive destruction of the aortic valve and the severity of the aortic insufficiency, the patient was evaluated for emergent replacement of the infected aortic valve; however, at that point in his clinical course, he was considered inoperable because of underlying medical point in disputes Despite the severity of his aortic insufficiency, the patient gradually improved in succession therapy with broad spectrum antibiotics. A follow-up echocardiogram upon the 30th hospital day showed progressive dilatation of the ventricle (69 mm) with preservation of the systolic function and reversion of the PMVC (Fig 1C) Of note, neither the patient's relations pressure nor heart rate changed significantly during the course of the illness. He was discharged from the hospital in useful condition after six weeks of antibiotic therapy.

Clinical Follow-up

Six month after discharge, the patient had his aortic valve replaced electively, because of progressive symptomatology related to aortic insufficiency; his echocardiogram at that time showed a normal Q-C interval of 007 s At the time of surgery there was no sign of active infection; the right coronary cusp of the aortic valve was perforated and flail, consistent with previous infective endocarditis. The pathologic report of this specimen indicated fibrosis, calcification and hyalinization of the tissue consistent with healed endocarditis.