In the Journals

Myocardial injury common among patients with chronic HCV

Patients with chronic HCV were prone to myocardial perfusion defects that responded to HCV treatment in a recent study.

Researchers performed ECG, echocardiography and myocardial perfusion imagery on 217 patients with chronic HCV and without overt heart disease symptoms to detect the presence and severity of myocardial injury. Two hundred patients received treatment with interferon (IFN) for 24 or 48 weeks, and were evaluated 2 weeks before, 2 weeks after and 6 months after therapy. Sustained viral response (SVR) was defined as undetectable HCV RNA 6 months after completing treatment.

Nine percent of patients in the cohort had abnormal ECGs, including 15 cases of sinus bradycardia and five with incomplete right bundle branch block before IFN treatment. Myocardial perfusion imaging indicated injury in 87% of patients, as represented by abnormal severity scores (SS). Histology activity index score, serum HCV RNA levels and rate of indocyanine green disappearance were independently associated with higher SS before IFN therapy via multiple linear regression (P<.0001 for all).

Among the 200 patients who completed treatment, SVR occurred in 92 patients and 57 experienced relapse; the remaining patients were considered nonresponsive. Participants who achieved SVR indicated significant improvement to SS after treatment and follow-up (P<.01). Patients who relapsed experienced an improvement to SS during treatment as HCV RNA disappeared, but returned to baseline SS at follow-up. No significant SS change occurred among nonresponders.

Rates of SS change from baseline were similar between patients who received 24 and 48 weeks of therapy. Differences in SS change according to response were significant for all comparisons, excluding those between patients who relapsed and those who were nonresponsive after 48 weeks of treatment (P=.2382).

“Our study is the first to demonstrate a relationship between chronic HCV infection and myocardial perfusion defects in a large number of patients,” the researchers wrote. “Although further studies are required to evaluate the exact relationship between chronic HCV infection and myocardial injury, our study suggests that HCV infection may play an important causal role in the pathogenesis of myocardial injury.”

Patients with chronic HCV were prone to myocardial perfusion defects that responded to HCV treatment in a recent study.

Researchers performed ECG, echocardiography and myocardial perfusion imagery on 217 patients with chronic HCV and without overt heart disease symptoms to detect the presence and severity of myocardial injury. Two hundred patients received treatment with interferon (IFN) for 24 or 48 weeks, and were evaluated 2 weeks before, 2 weeks after and 6 months after therapy. Sustained viral response (SVR) was defined as undetectable HCV RNA 6 months after completing treatment.

Nine percent of patients in the cohort had abnormal ECGs, including 15 cases of sinus bradycardia and five with incomplete right bundle branch block before IFN treatment. Myocardial perfusion imaging indicated injury in 87% of patients, as represented by abnormal severity scores (SS). Histology activity index score, serum HCV RNA levels and rate of indocyanine green disappearance were independently associated with higher SS before IFN therapy via multiple linear regression (P<.0001 for all).

Among the 200 patients who completed treatment, SVR occurred in 92 patients and 57 experienced relapse; the remaining patients were considered nonresponsive. Participants who achieved SVR indicated significant improvement to SS after treatment and follow-up (P<.01). Patients who relapsed experienced an improvement to SS during treatment as HCV RNA disappeared, but returned to baseline SS at follow-up. No significant SS change occurred among nonresponders.

Rates of SS change from baseline were similar between patients who received 24 and 48 weeks of therapy. Differences in SS change according to response were significant for all comparisons, excluding those between patients who relapsed and those who were nonresponsive after 48 weeks of treatment (P=.2382).

“Our study is the first to demonstrate a relationship between chronic HCV infection and myocardial perfusion defects in a large number of patients,” the researchers wrote. “Although further studies are required to evaluate the exact relationship between chronic HCV infection and myocardial injury, our study suggests that HCV infection may play an important causal role in the pathogenesis of myocardial injury.”