Publications

Antiretroviral therapy (ART) has been associated with a shift in the epidemiology of human immunodeficiency virus (HIV)-associated cardiomyopathy from a phenotype of primarily left ventricular (LV) systolic dysfunction to LV diastolic dysfunction (DD). Patients with HIV receiving ART have higher rates of DD compared with age-matched control subjects and develop DD at a younger age. However, little is known about the natural history and pathogenesis of DD in virally suppressed HIV-infected patients. Current evidence suggests that immune processes modulate the risk for cardiac involvement in HIV-infected persons. Ongoing inflammation appears to have myocardial effects, and accelerated myocardial fibrosis appears to be a key mediator of HIV-induced DD. The Characterizing Heart Function on Antiretroviral Therapy (CHART) study aims to systematically investigate determinants, mechanisms, and consequences of DD in HIV-infected patients. We will compare ART-treated virally suppressed HIV-infected individuals with and without DD and HIV- individuals with DD regarding (1) systemic inflammation, myocardial stress, and subclinical myocardial necrosis as indicated by circulating biomarkers; (2) immune system activation as indicated by cell surface receptors; (3) myocardial fibrosis according to cardiac magnetic resonance examination; (4) markers of fibrosis and remodeling, oxidative stress, and hypercoagulability; (5) left atrial function according to echocardiographic examination; (6) myocardial stress and subclinical necrosis as indicated by circulating biomarkers; (7) proteomic and metabolic profiles; and (8) phenotype signatures derived from clinical, biomarker, and imaging data.

Periprocedural management of anticoagulation for cardiac device implantation has evolved over the past 20 years. The traditional paradigm of vitamin K antagonist interruption with heparin bridging has now been shown to be less safe than continuation of vitamin K antagonists at therapeutic levels. Dual antiplatelet therapy during device implantation poses substantial risk but is often necessary. The safest dosing strategy for newer direct oral anticoagulants is still not clear.

BACKGROUND

It is currently unknown if the delay due to practical aspects associated with transfer of patients from a non-percutaneous coronary intervention (PCI) facility to a primary PCI facility is associated with adverse outcomes.

METHODS

We conducted a retrospective cohort study of all patients who presented with ST-segment elevation myocardial infarction (STEMI) and underwent primary PCI in 2 large regional STEMI centers in Massachusetts between January 2005 and June 2009. The cohort was divided into onsite patients who presented directly to the primary PCI center and transferred patients referred from another facility. The primary outcome was a composite of in-hospital major cardiovascular events (death, myocardial infarction, and stroke). Secondary outcomes were the individual components of the composite endpoint and bleeding complications.

RESULTS

The cohort included a total of 1236 patients. Among them, 426 (34%) patients were transferred patients and 810 (66%) were onsite patients. The median door to balloon time was significantly higher at for transferred patients (124 vs. 71 minutes). There was no significant difference in primary composite endpoint between the 2 groups (onsite 3.8% vs. transfer 5.3%, odds ratio 1.50, 95% confidence interval 0.79-2.84; P = 0.21). Adjusted risk estimates did not show a statistical difference in all-cause bleeding rates between the groups (onsite 10.1% vs. transfer 7.3%, odds ratio 0.68, 95% confidence interval 0.41-1.14; P = 0.14).

CONCLUSIONS

This study confirms that well-established and integrated regional STEMI programs provide equivalent care to transferred patients and onsite patients. Parameters beyond door to balloon times should be investigated for their contributions to improve patient outcomes.