Key result
HIV-positive patients with hypertension had a higher prevalence of left ventricular overload, strain, or hypertrophy on ECG compared to HIV-negative hypertensive controls (64.3% vs 35.7%).
Why the study?
Does HIV infection increase the prevalence of subclinical cardiovascular or renal organ damage in patients with hypertension?
Observational (n=305)
No
Does HIV infection increase the prevalence of subclinical cardiovascular or renal organ damage in patients with hypertension?
Absolute Event Rate: 64.3% vs 35.7%
HIV-positive patients with hypertension exhibit a premature and higher tendency toward subclinical cardiac organ damage, such as left ventricular hypertrophy and concentric remodeling, compared to HIV-negative hypertensive patients.
May support closer ECG monitoring in HIV-positive hypertensives; hypothesis-generating for independent HIV effects on cardiac damage.
Our objective has been the investigation of possible cardiovascular or renal organ damage in HIV patients with confirmed high blood pressure by means of instrumental cardiovascular investigation and renal function evaluation. A total of 265 consecutive patients accessing our outpatient facility were enrolled in the study. Patients with confirmed pathological pressure values or high normal values were submitted to clinical and instrumental monitoring by 24-hour ambulatory blood pressure monitoring (ABPM), to derivation of 12-lead ECG registration, to echocardiography and to epi-aortic vessel echo-color-Doppler. The ECG and echocardiographic data were compared to a control group of 40 hypertensive HIV-negative subjects. Renal damage was evaluated by means of the microalbuminuria/creatininuria ratio on a spot urine sample, plus 24-hour albuminuria and proteinuria measurements. 61 (23.0%) of the subjects examined were hypertensive: 24 (39.3%) had a previous hypertensive diagnosis but had never been treated for this condition, and 37 (60.7%) had a new diagnosis; In 100% of cases, 24-hour ABPM confirmed the hypertension and 27.8% of the patients resulted non-dippers. The ECG showed left ventricle overload, V4-V6 strain, or left ventricular hypertrophy in 64.3% of cases compared to 35.7% in the control group. Echocardiography demonstrated increasing in left ventricle parietal thickness with concentric remodeling and hypertrophy in 85.2% of patients. HIV-positive patients showed a statistically significant tendency to concentric remodeling and concentric hypertrophy, even in presence of mild hypertension. Echocolor-Doppler examination detected intima-media thickness > and/or carotid plaques in 72.1% of patients. Renal function seems spared in these subjects. Our data highlights the importance of investigating arterial hypertension among our patients as it is a frequently undiagnosed condition, and illustrates the utility of 24- hr ABPM to confirm hypertension and to identify the non-dipper subject. Moreover, the ECG, echocardiography and echocolor-Doppler examinations evidenced a premature tendency to organ damage in these patients that showed altered cardiac remodeling compared to those without HIV. This stresses the need for an early diagnosis, including a complete instrumental evaluation to properly identify organ damage even at a subclinical level.
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A 2013 study conducted an observational in HIV and hypertension (n=305). HIV infection vs. HIV-negative hypertensive subjects was evaluated on Left ventricle overload, V4-V6 strain, or left ventricular hypertrophy on ECG. HIV-positive patients with hypertension had a higher prevalence of left ventricular overload, strain, or hypertrophy on ECG compared to HIV-negative hypertensive controls (64.3% vs 35.7%).
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