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Verapamil improves the pacing-induced vasodilatation in symptomatic patients with hypertrophic cardiomyopathy
Paweł Petkow Dimitrow1, Marek Krzanowski, Janusz Grodecki
1Institute of Cardiology, Jagiellonian University School of Medicine, ul. Kopernika 17, 31-501 Kraków, Poland. dimitrow@mp.pl
Insights
Verapamil improves coronary blood flow in hypertrophic cardiomyopathy patients. The drug restored normal vasodilator response to pacing stress, suggesting impaired endothelium-dependent vasodilation in this condition.
Area of Science:
- Cardiology
- Pharmacology
- Medical Imaging
Background:
- Symptomatic hypertrophic cardiomyopathy (HCM) patients often exhibit impaired coronary vasodilator function.
- Endothelial dysfunction is a potential mechanism contributing to symptoms in HCM.
Purpose of the Study:
- To evaluate the effect of verapamil on diastolic coronary flow velocity and coronary vascular resistance during pacing in HCM patients.
- To assess if verapamil can restore normal vasodilator responses in HCM.
Main Methods:
- Transthoracic Doppler echocardiography was used to measure coronary flow velocity in the left anterior descending artery.
- Measurements were taken at baseline and during pacing in 14 HCM patients and 10 controls, with and without verapamil.
- Coronary vascular resistance changes were calculated during pacing.
Main Results:
- Verapamil significantly increased pacing-induced coronary flow velocity in HCM patients compared to off-verapamil (64.8% vs. 41.1%).
- HCM patients off verapamil showed a blunted response (41.1%) compared to controls (80.2%).
- Verapamil normalized the coronary vascular resistance decrease during pacing in HCM patients, similar to controls.
Conclusions:
- Symptomatic HCM patients have impaired endothelium-dependent vasodilation during pacing stress.
- Verapamil treatment effectively restores adequate vasodilator response to pacing in HCM patients.
- Verapamil may be a beneficial therapy for managing coronary circulatory dysfunction in HCM.
Abstract:
The purpose of the study was to assess the effect of verapamil on the response of diastolic coronary flow velocity and coronary vascular resistance to pacing in symptomatic patients with hypertrophic cardiomyopathy. In 14 patients with hypertrophic cardiomyopathy, the coronary flow velocity was detected in the left anterior descending coronary artery using transthoracic Doppler echocardiography. The peak diastolic coronary flow velocity and coronary vascular resistance was measured at baseline and during pacing. Changes of these parameters induced by the pacing (expressed as the percentage of baseline values) were compared on verapamil treatment and after verapamil withdrawal. The same measurements were obtained in ten control subjects. The results show that, in hypertrophic cardiomyopathy patients, increase in coronary flow velocity during pacing was significantly higher on than off verapamil therapy (64.8+/-32.5 vs. 41.1+/-21.3%, P<0.05). In control subjects, pacing-induced increase in coronary flow velocity was comparable to changes in coronary flow velocity in hypertrophic cardiomyopathy patients receiving verapamil (80.2+/-18.4 vs. 64.8+/-32.5%, P>0.05). After verapamil withdrawal in hypertrophic cardiomyopathy patients, coronary flow velocity increase during pacing was significantly lower than in control subjects (41.1+/-21.3 vs. 80.2+/-18.4%, P<0.05). During pacing the coronary vascular resistance decreased more on verapamil than after drug withdrawal (-34.7+/-11.7 vs. -24.6+/-12.9%, P<0.05). In control subjects the coronary vascular resistance decreased during pacing -38.6+/-6.3% to similar extent as in hypertrophic cardiomyopathy patients on verapamil. We can conclude that endothelium-dependent vasodilatation during pacing was impaired in symptomatic patients with hypertrophic cardiomyopathy. Verapamil treatment was able to restore adequate vasodilator response to pacing stress.
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