n the elderly population unrecognized heart failure is very common in patients with stable chronic obstructive pulmonary disease (COPD), 1 and the high prevalence of COPD, chronic heart failure (CHF) and their combination in this group [2][3][4] suggests that customized treatment may be required for such complicated disease status. We report using tiotropium, a non--adrenergic bronchodilator and novel M3 muscarinic receptor antagonist, for COPD complicated with CHF.
Case ReportA 77-year-old man was referred to hospital because of dyspnea on exertion. He was a heavy smoker of 60 cigarettes/day for 34 years and had CHF with history of hypertension and mild aortic regurgitation (AR) for 7 years, for which he was being treated with an angiotensin-converting enzyme inhibitor (temocapril, 2 mg) and loop diuretics (furosemide, 20 mg). His weight, blood pressure and heart rate were 56.8 kg, 124/64 mmHg and 80 beats/min, respectively. The breath sounds were decreased with fine rales in both of the posterior lung bases. Physical examination revealed no overt signs of right-sided heart failure, such as dilated jugular vein, hepatomegaly or peripheral edema.Chest X-ray showed increased fibro-linear infiltration in both lung bases ( Fig 1A) and ECG revealed sinus rhythm with complete right bundle branch block and high voltage in the chest leads ( Fig 1B). Laboratory investigations were normal except for a high concentration of brain natriuretic peptide (BNP: 222 pg/ml), which had been chronically elevated at approximately 200-300 pg/ml at least for 2 years.Echocardiography revealed left ventricular (LV) hypertrophy with an enlarged LV cavity and diffuse hypokinesis of the LV wall, with an ejection fraction (EF) of 27%. Right ventricular (RV) dimensions and wall motion were normal. The inferior vena cava showed respiratory movement and was not enlarged. Doppler echocardiography showed early diastolic transmitral flow velocity (E) of 1.2 m/s and the peak diastolic velocity during early filling of the longitudinal mitral annular motion (Ea) was 9.9 cm/s (Fig 2). The E/Ea ratio was 12.2, indicating high LV end-diastolic pressure (LVEDP). 5 The E/A ratio was 0.67, which indicated an abnormal relaxation pattern. Doppler echocardiographic estimated pressure gradient between right atrial (RA) and RV was 22 mmHg (Table 2) and systolic pulmonary artery (PA) pressure was 32 mmHg, indicating hemodynamic load on the right side of the heart. Right-heart catheterization, coronary angiography (CAG) and left ventriculography (LVG) were performed. Pulmonary capillary wedge pressure was 16 mmHg, PA pressure was 30/12 mmHg (mean PA pressure =22 mmHg), RA pressure was 4 mmHg and cardiac output was 5.6 L/min. Pulmonary vascular resistance was 86 dyne· s -1 ·cm -5 . CAG showed normal coronary arteries. LVG revealed diffuse hypokinesis with EF of 30% and mild AR. LVEDP was 14 mmHg. Therefore, we diagnosed left-sided heart failure and hemodynamic load on the right heart with neither pulmonary hypertension nor right-sided heart failure.Pulmonary func...