Elevated myocardial wall stress after percutaneous coronary intervention in acute ST elevation myocardial infraction is associated with increased mortality.

BACKGROUND: Despite early attempts to salvage myocardium-at-risk with percutaneous coronary intervention (PCI), changes in myocardial wall stress (MWS) leads to ventricular dilatation and dysfunction after acute ST-elevation myocardial infraction (STEMI). Whether this is transient or leads to long-term adverse outcomes major adverse cardiovascular events (MACE) is not known. We studied the association between MWS and MACE in patients after a successful PCI for acute STEMI. OBJECTIVES: To study the MWS in percutaneously revascularized STEMI patients in relation to all-cause mortality and MACE. METHODS: We prospectively enrolled 142 patients who presented to our tertiary care hospital with acute STEMI requiring emergent PCI. In addition to the standard clinical biomarkers, both end-systolic and end-diastolic MWS was calculated using our recently validated Echocardiographic indices. Patients were then prospectively followed up to an average of 16.5 (± 12.0) months to assess all-cause mortality and MACE. RESULTS: During the follow-up period, 9% of the patients died and 17% developed MACE. Patients who died had significantly elevated end-systolic WS compared to those who survived (mean ESWS, 80.01 ± 36.86 vs 59.28 ± 27.68). There was no significant difference in end-diastolic WS, left ventricular systolic function and peak troponin levels among survivors versus non-survivors. Elevated ESWS (>62.5 Kpa) and age remained the significant predictors of mortality on multivariate logistic analysis (OR 7.75, CI 1.33-73.86, P = .03; OR 1.16, CI 1.06-1.31, P = .002). CONCLUSION: Elevated ESWS measured by echocardiogram is associated with increased odds of long-term mortality in STEMI patients who have undergone emergent PCI. This finding can help clinicians to risk stratify high-risk patients.

Macrophage-specific protein perforin-2 is associated with poor neurological recovery and reduced survival after sudden cardiac arrest.

BACKGROUND: Biomarkers involved in inflammation and stress response were implicated in patients who were successfully resuscitated from out of hospital cardiac arrest (sR-OHCA). Here we report that macrophage-expressed gene, perforin-2, an evolutionarily conserved protein with membrane attack domain, is associated with poor neurological outcomes and mortality after sR-OHCA. OBJECTIVES: To examine the association between circulating perforin-2 protein measured within 6-h of sR-OHCA, mortality and neurological outcomes. METHODS: We prospectively enrolled 144 sR-OHCA patients from 4 different tertiary care centers. We measured perforin-2 and other conventional clinical biomarkers and compared between survivors vs. non-survivors. The neurological outcomes were dichotomized as poor or good according to the cereberal performance score. RESULTS: At the end of the hospital stay, 45% of the patients had died and 46% had poor neurological outcomes. Serum perforin-2 levels were significantly higher in patients with poor neurological recovery, compared to the ones with good neurological recovery (ng/mL, 13.7 ±â€¯45.9 vs. 1.2 ±â€¯7.0, p = 0.01). There were no differences in other routinely measured biomarkers and left ventricular ejection fraction. On multivariate logistic regression, elevated perforin-2 (OR: 12.78, 95% CI: 1.0-17.8, p = 0.02), comatose on presentation (OR: 27.82, 95% CI: 0.2-19.5, p = 0.02) and non-shockable rhythm (OR: 17.04, 95% CI: 0.7-15.7, p = 0.01) were the significant predictors of poor neurological outcome. CONCLUSIONS: This study reports a novel macrophage-expressed circulating biomarker perforin-2 to be strongly associated with reduced survival and poor neurological outcomes in sR-OHCA. These data can guide clinicians to prognosticate survival and neurological outcomes in sR-OHCA, and also form the basis for future therapeutic approaches.