Key result
Elevated end-systolic wall stress after STEMI PCI is linked to ~8-fold greater long-term mortality.
Why the study?
Whether post-PCI changes in myocardial wall stress in acute STEMI are transient or lead to long-term adverse outcomes and MACE is not known.
Does elevated end-systolic myocardial wall stress predict all-cause mortality and MACE in patients after successful PCI for acute STEMI?
Cohort (n=142)
No
Does elevated end-systolic myocardial wall stress predict all-cause mortality and MACE in patients after successful PCI for acute STEMI?
Elevated end-systolic myocardial wall stress measured by echocardiography after emergent PCI for STEMI is a strong independent predictor of long-term 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.
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Kattel et al. (2021) conducted a cohort in Acute ST-elevation myocardial infarction (STEMI) (n=142). Elevated end-systolic wall stress (ESWS >62.5 Kpa) vs. ESWS ≤62.5 Kpa was evaluated on All-cause mortality (OR 7.75, 95% CI 1.33-73.86, p=.03). Elevated end-systolic wall stress (>62.5 Kpa) after emergent PCI for STEMI was significantly associated with increased long-term mortality (OR 7.75; 95% CI 1.33-73.86; P=0.03).
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