A Lack of Reserve: Recognizing the Large Impact of Small Vessels in the Heart.

Information about a real patient is presented in stages (boldface type) to an expert clinician (Dr. Taqueti), who responds to the information, sharing her reasoning with the reader (regular type). A discussion by the authors follows. Patient presentation: A 67-year-old woman presented to the emergency department with escalating exertional chest pressure and dyspnea over the preceding week. Her symptoms are progressive such that she can no longer walk up a flight of stairs without chest discomfort. Resting and taking sublingual nitroglycerin provided mild improvement. There was no associated lightheadedness, palpitations or nausea. Over the preceding year, she had been able to walk five blocks without chest discomfort, although she reported angina at higher exertion. She has a history of coronary artery disease (CAD), diagnosed three years ago following stress myocardial perfusion imaging for evaluation of exertional chest pressure. Testing demonstrated a large area of inferior left ventricular (LV) ischemia, and she underwent percutaneous coronary intervention with placement of a drug-eluting stent to a 90% stenosis in the ostial right coronary artery (RCA). At the time of intervention, nonobstructive atherosclerotic plaques were noted in the mid RCA, proximal left anterior descending (LAD) artery, and proximal first diagonal branch artery. Six months following intervention, the patient was diagnosed with in-stent restenosis and underwent repeat coronary artery stenting. She continued to experience exertional chest pressure. Two weeks prior to presentation, she underwent repeat stress myocardial perfusion imaging with regadenoson single-photon emission computed tomography (SPECT), which demonstrated normal perfusion and LV systolic function. The patient’s medical history also includes hypertension, hyperlipidemia, diabetes, chronic kidney disease (CKD), obstructive sleep apnea (OSA) and osteoarthritis. She reported adherence to medications, including aspirin, clopidogrel, rosuvastatin, labetalol, hydralazine, isosorbide, metformin and insulin. She was a former smoker, and did not drink alcohol or use illicit drugs. She was a retired store clerk who lived with her daughter. The patient’s examination demonstrated an obese older woman who appeared comfortable at rest. Her vital signs revealed a heart rate of 60 bpm, blood pressure of 164/82 mm Hg bilaterally, oxygen saturation of 98% on ambient air, and a body mass index of 39.8 kg/m2. Jugular venous pressure was 8 cm and the apical impulse was normal in location and size. Auscultation revealed a regular rate and rhythm with normal S1 and S2 and clear lung fields bilaterally. Radial, femoral and dorsalis pedis pulses were of normal contour and intensity, and there was trace lower extremity pitting edema. Dr. Taqueti: A diabetic woman with a history of stable ischemic heart disease (SIHD) presents with escalating exertional angina and a markedly decreased exercise tolerance. Although her symptoms are progressive, an acute coronary syndrome must be excluded. Additional causes of chest pain, including pulmonary embolism, vascular dissection, myo/pericarditis, tachyarrhythmia, structural heart disease, coronary and esophageal spasm, and anemia, should be considered. Patient presentation (continued): A 12-lead ECG demonstrated normal sinus rhythm, prolonged QTc, criteria for LV hypertrophy, and nonspecific ST and T wave abnormalities (Figure 1), unchanged from prior tracings. Chest radiography was normal. Abnormal laboratory tests included glucose 217 mg/dL (reference 70–100), eGFR 46 mL/min (>60), hemoglobin 9.8 g/dL (11.5–16.4). Other labs, including electrolytes, N-terminal probrain natriuretic peptide, D-dimer, and thyroid-stimulating hormone, were normal. Three serial troponin T values measured over 24 hours were below assay. Recent lipid testing revealed a total cholesterol of 189 mg/dL, high-density lipoprotein 59 mg/dL, low-density lipoprotein (LDL) 117 mg/dL, triglycerides 140 mg/dL and a hemoglobin A1C of 8.4%. Transthoracic echocardiography demonstrated a small LV with mild concentric hypertrophy (12 mm wall thickness), LVEF of 0.65 without segmental wall motion abnormalities, grade II diastolic dysfunction, normal right ventricular size and systolic function, mild left atrial enlargement, normal valvular function, normal IVC size, and an estimated pulmonary artery systolic pressure of 36 mm Hg. Open in a separate window Figure 1. A 12-lead electrocardiogram on admission demonstrated normal sinus rhythm at 60 beats per minute, prolonged QTc of 491 ms, criteria for LV hypertrophy, and nonspecific ST and T wave abnormalities.