Bad news seemed to generate alarming symptoms in a 61-year-old woman. After learning of a stressful family situation, she presented to an outside hospital with acute, severe dyspnea and mild chest discomfort. Her past medical history included paroxysmal atrial fibrillation, remote pulmonary embolism, hypertension, hypothyroidism, and questionable mitral valve prolapse.
The patient also reported that she had a similar episode of dyspnea 5 years earlier. At that time, she underwent diagnostic cardiac catheterization with left ventriculography. Her coronary arteries were found to be normal, as was her left ventricular systolic function (estimated ejection fraction, 55%). She had no mitral regurgitation. From then on, she was maintained on candesartan, amiodarone, nebivolol, etilefrine, and rivaroxaban. She did not use tobacco or drink alcohol. Her brother had suffered a myocardial infarction but she did not recall at what age this had occurred.
At the start of the patient’s new hospital admission, she received 1.5 L of intravenous normal saline for a blood pressure of 72/50 mm Hg. She became hypoxic, requiring treatment with noninvasive positive pressure mechanical ventilation. Her laboratory measurements revealed an elevated creatinine level (1.7 mg/dL) and a normal lactate measurement (1.2 mmol/L). Troponin-I was undetectable. Her electrocardiogram findings included atrial fibrillation with nonspecific T-wave changes, and a transthoracic echocardiogram demonstrated a left ventricular ejection fraction of 55%-60%, no wall-motion abnormalities, a moderately dilated left atrium with elevated left atrial pressure, moderate tricuspid regurgitation, severe pulmonary hypertension, and severe mitral regurgitation. The patient was then transferred to our hospital.
Assessment
Upon arrival, the patent’s pulse was 86 beats per minute, her blood pressure was 99/70 mm Hg, her respiratory rate was 21 breaths per minute, and her oxygen saturation was 98%, with bilevel positive airway pressure support at 15/5 cm H2O and 40% FiO2. She had no peripheral edema, and her jugular venous pressure was not elevated when lying at a 30-degree angle. Her cardiopulmonary examination findings were notable for diffuse rales bilaterally and an irregularly irregular rhythm. No murmurs were heard. Chest radiography disclosed findings consistent with pulmonary edema, and repeat laboratory measurements showed an improvement in creatinine level to 1.1 mg/dL, a lactate level of 1.7 mmol/L, and troponin-I remained imperceptible. The patient was given intravenous diuretics and weaned to nasal cannula.
When transthoracic echocardiography was repeated at our institution, it indicated that left ventricular ejection fraction (55%-60%), left ventricular function, wall motion, and wall thickness were all normal, while the right ventricular and left atrial chambers were mildly dilated. Most striking, the patient’s mitral regurgitation was mild, a significant improvement from her prior study. The mitral valve itself was structurally normal with mild diffuse sclerotic or myxomatous thickening of the leaflets. Minimal prolapse or buckling of the anterior leaflet was evident, but she did not meet criteria for mitral valve prolapse. Coronary angiography, left ventriculography, and right heart catheterization indicated that her filling pressures were normal, she had no significant coronary artery disease, and only trace mitral regurgitation was occurring.
A transesophageal echocardiogram discerned mild mitral regurgitation without uncovering any structural valvular abnormalities (Figure 1). In light of the discrepant and clinically significant differences in mitral regurgitation found on the 2 transthoracic echocardiograms, the patient underwent another while medications that affect cardiac hemodynamics were administered (Table, Figure 2). At baseline, the third transthoracic echocardiogram demonstrated normal left ventricular size and function with mild-to-moderate mitral regurgitation, an estimated stroke volume of 62 mL/beat, and mild tricuspid regurgitation with an estimated right ventricular systolic pressure of 26 mm Hg.
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-David Furfaro, MD, Karly Murphy, MD, Jordan Chaisson, MD, Jose Madrazo, MD, Sammy Zakaria, MD, MPH
This article originally appeared in the August 2016 issue of The American Journal of Medicine.
