Wide access to highly effective combination antiretroviral therapy (ART) has ostensibly changed HIV infection status in many parts of the world from a fatal diagnosis to a chronic condition. However, extended life expectancy comes with long-term noninfectious comorbidities (NICMs), such as cardiovascular disease (CVD) (1). Prior studies have demonstrated that CVD is more common among the HIV-infected population than HIV-uninfected controls (2,3). This increased risk was partly explained by traditional risk factors of CVD such as smoking, diabetes, age, gender, as well as HIV infection itself, such as CD4 cell count and/or viral load, which is known to cause inflammation response by oxidative stress or coagulation disorders (4-6). However, the relative contributions of conventional cardiovascular risk factors, metabolic side effects of ART, and HIV infection itself on CVD risk are difficult to identify, as these factors frequently occur simultaneously (7). Due to its wide availability, low cost and the accumulating evidence that electrocardiographic (ECG) abnormalities are predictive of incident cardiovascular events in the general population (8), the 12-lead electrocardiogram is a very useful non-invasive tool for evaluation of cardiac disorders and risks in clinical settings. Several typical ECG parameters, including resting heart rate and markers of abnormal cardiac depolarization/repolarization, have been previously reported to be associated with increased risk of sudden cardiovascular death (SCD) (9,10). Cardiovascular involvement in HIV/AIDS was recognized as part of the pandemic and a wide spectrum of cardiovascular abnormalities including corrected QT (QTc) prolongation, widened spatial QRS-T angle, ST-segment depressions, T-wave changes, and resting heart rate have been widely reported (11-13). Moreover, the association between age, obesity, alcohol consumption, lower CD4 cell count and LV diastolic dysfunction and ECG abnormalities were documented among HIV-positive patients (14,15).