Prolonged QT predicts prognosis in COVID-19.

BACKGROUND: Coronavirus disease-2019 (COVID-19) causes severe illness and multi-organ dysfunction. An abnormal electrocardiogram is associated with poor outcome, and QT prolongation during the illness has been linked to pharmacological effects. This study sought to investigate the effects of the COVID-19 illness on the corrected QT interval (QTc). METHOD: For 293 consecutive patients admitted to our hospital via the emergency department for COVID-19 between 01/03/20 -18/05/20, demographic data, laboratory findings, admission electrocardiograph and clinical observations were compared in those who survived and those who died within 6 weeks. Hospital records were reviewed for prior electrocardiograms for comparison with those recorded on presentation with COVID-19. RESULTS: Patients who died were older than survivors (82 vs 69.8 years, p < 0.001), more likely to have cancer (22.3% vs 13.1%, p = 0.034), dementia (25.6% vs 10.7%, p = 0.034) and ischemic heart disease (27.8% vs 10.7%, p < 0.001). Deceased patients exhibited higher levels of C-reactive protein (244.6 mg/L vs 146.5 mg/L, p < 0.01), troponin (1982.4 ng/L vs 413.4 ng/L, p = 0.017), with a significantly longer QTc interval (461.1 ms vs 449.3 ms, p = 0.007). Pre-COVID electrocardiograms were located for 172 patients; the QTc recorded on presentation with COVID-19 was longer than the prior measurement in both groups, but was more prolonged in the deceased group (448.4 ms vs 472.9 ms, pre-COVID vs COVID, p < 0.01). Multivariate Cox-regression analysis revealed age, C-reactive protein and prolonged QTc of >455 ms (males) and >465 ms (females) (p = 0.028, HR 1.49 [1.04-2.13]), as predictors of mortality. QTc prolongation beyond these dichotomy limits was associated with increased mortality risk (p = 0.0027, HR 1.78 [1.2-2.6]). CONCLUSION: QTc prolongation occurs in COVID-19 illness and is associated with poor outcome.

Prognostic value of blood pressure measured during hospitalization after acute myocardial infarction: an insight from survival trials.

BACKGROUND: The prognostic value of blood pressure measured during hospitalization after acute myocardial infarction (MI) has not been investigated, particularly with regard to arrhythmic death. METHODS: A total of 3311 placebo patients (2612 men, median age 64 years; range 23-92) from the EMIAT, CAMIAT, SWORD, TRACE and DIAMOND-MI studies with left ventricular ejection fraction less than 40% or asymptomatic ventricular arrhythmia surviving more than 45 days after MI were pooled. Systolic and diastolic blood pressures and pulse pressures were measured soon after MI (median 6 days, range 0-53 days). Mortality up to 2 years was examined using Cox regression. RESULTS: At the 2-year follow-up, after adjustment for age, sex, smoking, previous MI, hypertension, heart rate, New York Heart Association functional class, baseline treatments, study effect and diastolic blood pressure, reduced systolic blood pressure measured during hospitalization after acute MI significantly increased the risk of all-cause mortality [hazard ratio (HR) for 10% increase in systolic blood pressure 0.80, 95% confidence interval (CI) 0.71-0.90; P < 0.001] and arrhythmic mortality (HR 0.73, 95% CI 0.61-0.86; P = 0.001). Reduced diastolic blood pressure significantly increased the risk of all-cause mortality (HR 0.87, 95% CI 0.77-0.98; P = 0.02) and arrhythmic mortality (HR 0.80, 95% CI 0.68-0.93; P = 0.005). CONCLUSION: In post-MI patients with left ventricular ejection fraction less than 40% or asymptomatic ventricular arrhythmia, reduced blood pressure measured during hospitalization after MI significantly predicts all-cause mortality and arrhythmic mortality, and can be reliably used to identify patients who are at risk of dying after MI.

Prognostic impact of demographic factors and clinical features on the mode of death in high-risk patients after myocardial infarction--a combined analysis from multicenter trials.

BACKGROUND: Contemporary information is lacking on the effect of demographic features and clinical features on the specific mode of mortality after myocardial infarction (MI) in the thrombolytic era. HYPOTHESIS: The aims of this study were (1) to examine the risk and trend of a different mode of mortality (i.e., all-cause, arrhythmic, and nonarrhythmic cardiac mortality) in high-risk patients post MI with reduced left ventricular ejection fraction (LVEF) or ventricular arrhythmias; and (2) to assess the predictive value of demographic and clinical variables in the prediction of specific modes of death in high-risk patients post MI in the thrombolytic era. METHODS: In all, 3,431 patients receiving placebo (2,700 men, median age 64 +/- 11 years) from the EMIAT, CAMIAT, SWORD, TRACE, and DIAMOND-MI studies, with LVEF < 40% or ventricular arrhythmia were pooled. Risk factors for mortality among patients surviving > or = 45 days after MI up to 2 years were examined using Cox regression. Short-term survival (from onset of MI to Day 44 after MI) was also examined for TRACE and DIAMOND-MI, in which patients were recruited within 2 weeks of MI. RESULTS: After adjustment for treatment and study effects, age, previous MI/angina, increased heart rate, and higher New York Heart Association functional class increased the risk of all-cause, arrhythmic, and cardiac mortality. Male gender, history of hypertension, low baseline systolic blood pressure, and Q wave were predictive of all-cause and arrhythmic mortality, whereas diabetes was only predictive of all-cause mortality. Smoking habit and atrial fibrillation had no prognostic value. Similar parameters were also predictive of short-term mortality, but not identical. CONCLUSIONS: Our study has shown that in high-risk patients post MI, who have been preselected using LVEF or frequent ventricular premature beats, demographic and clinical features are powerful predictors of mortality in the thrombolytic era. We propose that demographic and clinical factors should be considered when designing risk stratification or survival studies, or when identifying high-risk patients for prophylactic implantable cardiodefibrillator therapy.