Explaining Unexplained Dyspnea

Abstract

A 63-year-old man was evaluated in consultation for unexplained dyspnea. At the time of the initial clinical encounter at our institution, the patient endorsed a 10-year history of progressive exertional dyspnea, which had become debilitating over the preceding 3 months and was characterized by shortness of breath accompanying subtle physical activities such as tying shoelaces. The patient underwent multiple hospital admissions reportedly for the treatment of congestive heart failure ascribed to impaired left ventricular (LV) diastolic function. Review of systems identified postural dizziness and history of near syncope, possible nocturnal dyspnea, and peripheral neuropathy, but not cardiac angina, orthopnea, nocturia, edema, cough, palpitations, syncope, claudication, or other cardiopulmonary symptoms. He related that he was first noted to have a cardiac murmur detected 4 decades previously during a military service physical examination but that the murmur was not characterized further and that he served in the Vietnam conflict without functional limitation. The patient’s relevant medical history included rate-controlled atrial fibrillation, 90 pack-year tobacco use (3 packs daily between 21 and 51 years of age), dyslipidemia, systemic hypertension, type 2 diabetes mellitus, moderate chronic obstructive pulmonary disease, obstructive sleep apnea not currently treated, and gastrointestinal bleed caused by colon cancer treated with hemicolectomy 11 years earlier. There was no illicit drug use, but a remote history of heavy alcohol consumption was reported. Family history was unremarkable except that his father died at 55 years of age of myocardial infarction. Medications included aspirin 81 mg daily, warfarin 2 mg daily, losartan 50 mg daily, metoprolol tartrate 25 mg twice daily, simvastatin 10 mg daily, fenofibrate 48 mg daily, albuterol inhaler 90-μg puffs as needed, and gabapentin 300 mg 3 times daily.

Sinus Venosus Atrial Septal Defect Complicated by Eisenmenger Syndrome and the Role of Vasodilator Therapy

“…The superior SVASD comprises 5–10% of cases of ASD [1, 2]. The interatrial left-to-right shunting leads to right ventricular volume overload and increases in pulmonary blood flow and pulmonary vascular resistance [1, 3]. The left-to-right shunting is significant when the ratio of Q P / Q S is greater than 1.5 : 1, or when a patient develops dilation of the right heart chambers [2].…”

“…The left-to-right shunting is significant when the ratio of Q P / Q S is greater than 1.5 : 1, or when a patient develops dilation of the right heart chambers [2]. The right ventricular volume overload results in right ventricular dilation, pulmonary vascular modeling, pulmonary hypertension, and ultimately Eisenmenger physiology, which is an irreversible right-to-left shunt [3] as illustrated in this case.…”

“…It usually coexists with partial anomalous pulmonary venous return (PAPVR), which leads to additional left-to-right shunting. SVASD is generally unrecognized until the fifth decade of life when it presents as right heart failure and/or pulmonary hypertension [3]. SVASDs are usually located near the superior or inferior vena cava entry into the right atrium.…”

“…SVASDs are usually located near the superior or inferior vena cava entry into the right atrium. This interatrial communication leads to volume overload, right-sided chamber dilation, and ultimately pulmonary hypertension [1, 3]. In this paper, we present a case of pulmonary artery hypertension and Eisenmenger syndrome due to a superior form of SVASD.…”

Progressive Onset of Extracardiac and Myocardial Symptoms

“…6,7 Even though the cardiac examination and echocardiographic findings could be consistent with acute or chronic PE, peripheral examination revealed no stigmata of peripheral venous thromboembolism. Acute PE is less likely with a negative CT, but the presentation and echocardiographic findings could be consistent with chronic thromboembolic disease; typically, this requires a ventilation-perfusion scan to detect chronic perfusion mismatch, which can evolve into chronic thromboembolic pulmonary hypertension.…”