Pharmacotherapy reduces conduction system disease risk
medwireNews: Lisinopril therapy significantly reduces incident conduction system disease, indicates a post-hoc analysis of ALLHAT data.
Among 21,004 individuals aged 55 years and older with hypertension and at least one other cardiac risk factor, lisinopril treatment was associated with a significant 19% reduction in the onset of conduction abnormalities on 12-lead electrocardiogram (ECG) compared with chlorthalidone.
Gregory Marcus (University of California, San Francisco, USA) and colleagues note that this reduction in risk was not explained by lisinopril’s antihypertensive effects, which were inferior to those of chlorthalidone.
Rather, they suggest that the drug’s ability to mitigate left ventricular hypertrophy, which was the predominant independent risk factor for conduction system disease, “may provide an explanation for the efficacy of ACE inhibitors beyond their antifibrotic effects.”
Other independent risk factors included increased age, being male, smoking and having diabetes, the team reports in JAMA Internal Medicine.
In all, 5542 patients were randomly assigned to receive lisinopril, 9726 to receive chlorthalidone and 5736 amlodipine besylate. Patients with elevated fasting low-density lipoprotein cholesterol levels were also given pravastatin or treated with standard hyperlipidaemia treatment.
ECGs carried out at enrolment and every 2 years during an average follow-up of 5 years showed the development of conduction defects in 1114 individuals, including right bundle branch block (RBBB) in 570, left bundle branch block (LBBB) in 389 and intraventricular conduction delay in 155. The overall incidence per 1000 person–years was 13.0 for any conduction abnormality, 6.6 for RBBB and 4.5 for LBBB.
None of the patients developed first-degree atrioventricular block, left anterior fascicular block or incomplete bundle branch block.
Only lisinopril offered treatment benefit, the researchers note; neither amlodipine nor pravastatin therapy was associated with a reduced incidence of conduction system disease.
An unexpected finding was the reduced risk for incident conduction system disease among Black versus White individuals, which the team says is of interest in light of growing evidence suggesting the risk of atrial fibrillation is also reduced.
“While speculative these findings raise the possibility that a singular mechanism (eg, accelerated myocardial fibrosis) could explain the heightened propensity for atrial fibrillation and conduction system disease observed in white compared with black populations”, they say.
Congratulating Marcus and team on their research in a related commentary, David Maron (Stanford University, California, USA) and colleagues say that important next steps would be to confirm the finding, better define those individuals most likely to benefit and determine whether pharmacological treatment can affect existing conduction abnormalities, including the need for pacemaker implantation.
“This is indeed an exciting prospect!” they conclude.
By Lucy Piper
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