Incidence and risk factors of asymptomatic first-dose hypotension with angiotensin-converting enzyme inhibitors in chronic heart failure due to systolic dysfunction.

BACKGROUND: In practice, chronic heart failure is often not treated with angiotensin-converting enzyme inhibitors. One reason is the fear of first-dose hypotension. In the majority of patients, this condition is asymptomatic and the consequences are unexpected. Presently, little is known of its epidemiology. METHODS AND RESULTS: This was a prospective, 48-hour observational study of 160 patients with chronic heart failure due to systolic dysfunction, previously untreated with angiotensin-converting enzyme inhibitors, randomly drawn from the clinical practice of selected cardiologists across India. The primary outcome was a change in the mean arterial pressure during the first 24-hours after the first dose of an angiotensin-converting enzyme inhibitor. In 131/160 patients (81.9%) with no hypotensive symptoms, the incidence of first-dose hypotension (maximum 24-hour fall in mean arterial pressure greater than 10% from baseline) was 56/131 (42.7%). Pre-treatment diastolic pressure had a negative, independent association with 24-hour change in mean arterial pressure, accounting for 29% (R2=0.29, p<0.01) of its variability, and its predictive value was greater with pro-drug angiotensin-converting enzyme inhibitors. The incidence of first-dose hypotension increased from 1 patient (4.8%) at a pre-treatment diastolic pressure of 50-70 mmHg to 35 patients (42.7%) at 71-90 mmHg, p<0.01. CONCLUSIONS: The incidence of first-dose hypotension with angiotensin-converting enzyme inhibitors in outpatients with chronic heart failure due to systolic dysfunction is high. Pre-treatment diastolic pressure is an independent risk factor, and its predictive value increases with pro-drug angiotensin-converting enzyme inhibitors. This could help physicians to anticipate asymptomatic first-dose hypotension and increase the utilization of these agents in heart failure.

Chlamydia pneumoniae infection and nonspecific aortoarteritis: search for a link with a nonatherosclerotic inflammatory arterial disease.

BACKGROUND: The association between Chlamydia pneumoniae infection and atherosclerosis has gained recognition. However, the nature of this association is controversial. The infective link may not be specific for atherosclerosis and may also exist in other nonatherosclerotic arterial diseases. We investigated patients with nonspecific aortoarteritis for serological evidence of prior Chlamydia pneumoniae infection. METHODS AND RESULTS: Fifty patients each of nonspecific aortoarteritis and coronary artery disease with angiographic evidence of significant (>70%) coronary artery lesions were tested for the presence of IgG antibodies against Chlamydia pneumoniae by micro-immunofluorescence assay and compared with 50 age- and sex-matched normal healthy controls. The number of patients with nonspecific aortoarteritis who tested positive for Chlamydia pneumoniae antibodies (IgG) was not significantly different from controls (8 v. 7, p=ns). The mean titer amongst positive subjects in the two groups was also similar (1:40+/-40 v. 1:50+/-25; p=ns). Patients with coronary artery disease were significantly older than patients with nonspecific aortoarteritis and controls (53.2+/-5.8 v. 21.2+/-9.9 years and 24.5+/-5.2 years, p<0.01 for both) and showed a higher seroprevalence of prior Chlamydia pneumoniae infection (18 v. 8 and 7, p < 0.05 for both). The mean IgG titers of patients with coronary artery disease who tested positive were also significantly higher than the other two groups (1:98+/-34 v. 1:40+/-40, p<0.001 and 1:98+/-34 v. 1:50+/-25, p<0.01, respectively). CONCLUSIONS: In patients with nonspecific aortoarteritis, the seroprevalence of prior Chlamydia pneumnoniae infection is not more than that in healthy individuals of the same age group, but is significantly lesser than that in patients with coronary artery disease. Thus Chlamydia pneumoniae infection may not be associated with all forms of chronic inflammatory arterial lesions.