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• Addition of renal function may be valuable for risk stratification. • This study included 12,449 low-risk patients with chest pain. • R 2 CHA 2 DS 2 -VASc score predicted acute coronary syndrome and mortality 30 days and 1 year after discharge. Chest-pain patients with no evidence of acute coronary syndrome might still be at risk for adverse outcomes. Adding renal function to the classic scoring of CHADS and CHA 2 DS 2 VASC may improve risk stratification of chest-pain patients discharged from internal medicine wards after acute coronary syndrome (ACS) rule-out. We accessed medical records of patients admitted to internal medicine wards during 2010–2016 and discharged following ACS rule-out. A R 2 CHA 2 DS 2 -VASc score model that included higher scores as kidney function deteriorated was calculated and compared to CHADS and CHA 2 DS 2 VASC scores. The primary endpoint was the composite of 30-day ACS and mortality. One-year ACS and 1-year mortality were the secondary endpoints. The study included 12,449 patients, stratified into three risk groups according to their R 2 CHA 2 DS 2 -VASc score. Participants were stratified into 3 groups according to R 2 CHA 2 DS 2 -VASc score. R 2 CHA 2 DS 2 -VASc score predicted better the composite outcome of ACS and 30-day and 1-year mortality after discharge (OR: 4, 95%, CI 2.3–7, p < 0.01 and OR: 13.3, 95% CI 7.8–22.7, p < 0.01, respectively). Receiver operating characteristic curve analysis showed better risk stratification of the R 2 CHA 2 DS 2 -VASc compared with both CHADS and CHA 2 DS 2 VASC score. The R 2 CHA 2 DS 2 -VASc score is a better predictor of short- and long-term cardiovascular morbidity and mortality after hospital discharge. [ABSTRACT FROM AUTHOR]

• Medical records of ambulatory patients with heart failure were reviewed. • Among 814 patients, 464 (57%) had non-coronary cardiac calcifications. • Patients with calcifications had more hospitalizations for heart failure. • The OR for all-cause death, HF hospitalizations, and the composite endpoint were greater in patients with calcifications. • Calcifications should be included in risk stratification for heart failure. Calcium deposits on heart valves are considered a local manifestation of atherosclerosis and are associated with poor cardiovascular outcomes. The clinical significance of cardiac calcifications among heart failure (HF) patients, as assessed by echocardiography, is unknown. This study evaluated associations of cardiac calcifications with mortality and hospital admissions in this specific population. Medical records of all patients who initiated ambulatory surveillance at our HF clinic during 2011–2018 were reviewed. Calcifications in the aortic valve, aortic root, or the mitral valve were evaluated. Patients with moderate to severe regurgitation or stenosis of the aortic or mitral valves were excluded. The primary endpoint was the composite of long-term all-cause mortality and HF hospitalizations. Secondary endpoints were long-term all-cause mortality and more than one hospitalization due to HF. This retrospective study included 814 patients (mean age 70.9 ± 13 years, 63.2% male). Of the total cohort, 350 (43%) had no cardiac calcifications and 464 (57%) had at least 1 calcified site. Considering the patients with no calcification as the reference group yielded a higher adjusted odds ratios for the composite endpoint, all-cause death, and recurrent HF hospitalizations, among patients with any cardiac calcification (OR = 1.68, 95%CI = 1.1–2.5, p = 0.01, OR=1.61, 95%CI = 1.1–2.3, p < 0.01, and OR = 1.50, 95%CI = 1.1–2.2, p < 0.01, respectively). We found an independent association between cardiac calcifications and the risk of death and HF hospitalizations among ambulatory HF patients. Cardiac calcifications evaluated during routine echocardiography may contribute to the risk stratification of patients with HF. [ABSTRACT FROM AUTHOR]

Background: Cardiac arrest may result from seemingly innocuous medications that do not necessarily have cardiac indications. The best-known example is the drug-induced long QT syndrome. A less known but not necessarily less important form of drug-induced proarrhythmia is the drug-induced Brugada syndrome.Objective: The purpose of this study was to identify clinical and ECG risk markers for drug-induced Brugada syndrome.Methods: Reports of drug-induced Brugada syndrome recounted by an international database (http://www.brugadadrugs.org) were reviewed to define characteristics that identify patients prone to developing this complication. For each patient with drug-induced Brugada syndrome who had an ECG recorded in the absence of drugs, we included 5 healthy controls matched by gender and age. All ECGs were evaluated for Brugada-like abnormalities.Results: Seventy-four cases of drug-induced Brugada syndrome from noncardiac medications were identified: 77% were male, and drug toxicity was involved in 46%. Drug-induced Brugada syndrome from oral medications generally occurred weeks after the initiation of therapy. Mortality was 13%. By definition, all cases had a type I Brugada pattern during drug therapy. Nevertheless, their ECG in the absence of drugs was more frequently abnormal than the ECG of controls (56% vs 33%, P = .04).Conclusion: Drug-induced Brugada syndrome from noncardiac drugs occurs predominantly in adult males, is frequently due to drug toxicity, and occurs late after the onset of therapy. Minor changes are frequently noticeable on baseline ECG, but screening is impractical because of a prohibitive false-positive rate. [ABSTRACT FROM AUTHOR]

Background: Specific T-wave patterns on the resting electrocardiogram (ECG) aid in diagnosing long QT syndrome (LQTS) and identifying the specific genotype. However, provocation tests often are required to establish a diagnosis when the QT interval is borderline at rest.Objective: The purpose of this study was to determine whether T-wave morphology changes provoked by standing aid in the diagnosis of LQTS and determination of the genotype.Methods: The quick-standing test was performed by 100 LQTS patients (40 type 1 [LQT1], 42 type 2 [LQT2], 18 type 3 [LQT3]) and 100 controls. Logistic regression was used to determine whether T-wave morphology changes provoked by standing added to the already established diagnostic value of QTc stretching in identifying LQTS.Results: During maximal QT stretching, the T-wave morphologies that best discriminated LQTS from controls included "notched," "late-onset," and "biphasic" T waves. These 3 categories were grouped into a category named "abnormal T-wave response to standing." During quick standing, a QTc stretched ≥490 ms increased the odds of correctly identifying LQTS. T-wave morphology changes provoked by standing were most helpful for identifying LQT2, less helpful for LQT1, and least helpful for LQT3.Conclusion: The sudden heart rate acceleration produced by abrupt standing not only increases the QTc but also exposes abnormal T waves that are valuable for diagnosing LQTS. [ABSTRACT FROM AUTHOR]

Background: Fever is known to unmask the Brugada pattern on the electrocardiogram (ECG) and trigger ventricular arrhythmias in patients with Brugada syndrome. Genetic studies in selected cases with fever-induced Brugada pattern have identified disease-causing mutations. Thus, “fever-induced Brugada” is a recognized clinical entity. However, its prevalence has not been systematically evaluated. Objective: The purpose of this study was to assess the prevalence of Brugada pattern in consecutive patients with fever. Methods: ECGs of patients with fever admitted to the emergency department were evaluated for the presence of Brugada pattern and compared with ECGs of consecutive nonfebrile patients. Results: ECGs of 402 patients with fever and 909 without were evaluated. Type I Brugada pattern was 20 times more common in the febrile group than in the afebrile group (2% vs 0.1%, respectively, P = .0001). All patients with fever-induced type I Brugada pattern were asymptomatic and remained so during 30 months of follow-up. Conclusion: Type I Brugada pattern is definitively more common among patients with fever, suggesting that asymptomatic Brugada syndrome is more prevalent than previously estimated. [Copyright &y& Elsevier]