Torsades de pointes and myocardial infarction following reversal of supraventricular tachycardia with adenosine: a case report.

Adenosine is an antiarrhythmic drug that slows conduction through the atrioventricular node and acts as a coronary blood vessel dilator. This case report highlights two unusual life-threatening events following the use of adenosine to revert supraventricular tachycardia in a structurally normal heart: non-sustained polymorphic ventricular tachycardia and myocardial infarction. A 46-year-old woman presented to the emergency department with a two-hour history of palpitations and was diagnosed with supraventricular tachycardia. Vagal maneuvers were ineffective, and after intravenous adenosine administration, the patient presented with chest pain and hypotension. The rhythm degenerated into non-sustained polymorphic ventricular tachycardia and spontaneously reverted to sinus rhythm with ST elevation in lead aVR and ST depression in the inferior and anterolateral leads. The patient spontaneously recovered within a few minutes. Despite successful arrhythmia reversal, the patient was admitted to the intensive care unit because of an infarction without obstructive atherosclerosis. This report aims to alert emergency physicians about the potential complications associated with supraventricular tachycardia and its reversal with adenosine.

Myocardial microstructure assessed by T1 mapping after on-pump and off-pump coronary artery bypass grafting.

Background: The correlation between the release of cardiac biomarkers after revascularization, in the absence of late gadolinium enhancement (LGE) or myocardial edema, and the development of myocardial tissue damage remains unclear. This study sought to identify whether the release of biomarkers is associated with cardiac damage by assessing myocardial microstructure on T1 mapping after on-pump (ONCAB) and off-pump coronary artery bypass grafting (OPCAB). Methods: Seventy-six patients with stable multivessel coronary artery disease (CAD) and preserved systolic ventricular function were included. T1 mapping, high-sensitive cardiac troponin I (cTnI), creatine kinase myocardial band (CK-MB) mass, and ventricular dimensions and function were measured before and after procedures. Results: Of the 76 patients, 44 underwent OPCAB, and 32 ONCAB; 52 were men (68.4%), and the mean age was 63±8.5 years. In both OPCAB and ONCAB the native T1 values were similar before and after surgeries. An increase in extracellular volume (ECV) values after the procedures was observed, due to the decrease in hematocrit levels during the second cardiac resonance. However, the lambda partition coefficient showed no significant difference after the surgeries. The median peak release of cTnI and CK-MB were higher after ONCAB than after OPCAB [3.55 (2.12-4.9) vs. 2.19 (0.69-3.4) ng/mL, P=0.009 and 28.7 (18.2-55.4) vs. 14.3 (9.3-29.2) ng/mL, P=0.009, respectively]. Left ventricular ejection fraction (LVEF) was similar in both groups before and after surgery. Conclusions: In the absence of documented myocardial infarction, T1 mapping did not identify structural tissue damage after surgical revascularization with or without cardiopulmonary bypass (CPB), despite the excessive release of cardiac biomarkers.

Abnormal release of cardiac biomarkers in the presence of myocardial oedema evaluated by cardiac magnetic resonance after uncomplicated revascularization procedures.

AIMS: To analyse the association of myocardial oedema (ME), observed as high T2 signal intensity (HT2) in cardiac magnetic resonance imaging, with the release of cardiac biomarkers, ventricular ejection, and clinical outcomes after revascularization. METHODS AND RESULTS: Patients with stable coronary artery disease with the indication for revascularization were included. Biomarker levels [troponin I (cTnI) and creatine kinase MB (CK-MB)] and T2-weighted and late gadolinium enhancement (LGE) images were obtained before and after the percutaneous or surgical revascularization procedures. The association of HT2 with the levels of biomarkers, with and without LGE, evolution of left ventricular ejection fraction (LVEF), and 5-year clinical outcomes were assessed. A total of 196 patients were divided into 2 groups: Group 1 (HT2, 40) and Group 2 (no HT2, 156). Both peak cTnI (8.9 and 1.6 ng/mL) and peak CK-MB values (44.7 and 12.1 ng/mL) were significantly higher in Group 1. Based on the presence of new LGE, patients were stratified into Groups A (no HT2/LGE, 149), B (HT2, 9), C (LGE, 7), and D (both HT2/LGE, 31). The peak cTnI and CK-MB values were 1.5 and 12.0, 5.4 and 44.7, 5.0 and 18.3, and 9.8 and 42.8 ng/mL in Groups A, B, C, and D, respectively, and were significantly different. The average LVEF decreased by 4.4% in Group 1 and increased by 2.2% in Group 2 (P = 0.057). CONCLUSION: ME after revascularization procedures was associated with increased release of cardiac necrosis biomarkers, and a trend towards a difference in LVEF, indicating a role of ME in cardiac injury after interventions.

Association of Longitudinal Values of Glycated Hemoglobin With Cardiovascular Events in Patients With Type 2 Diabetes and Multivessel Coronary Artery Disease.

Importance: Glycated hemoglobin (HbA1c) values are used to guide glycemic control, but in patients with type 2 diabetes and multivessel coronary artery disease (CAD), the association of the longitudinal values of HbA1c with cardiovascular outcomes is unclear. Objective: To assess whether longitudinal variation of HbA1c is associated with cardiovascular events in long-term follow-up among patients with diabetes and multivessel CAD. Design, Setting, and Participants: This cohort study included 888 patients with type 2 diabetes and multivessel CAD in the Medicine, Angioplasty, or Surgery Study (MASS) Registry of the Heart Institute of the University of São Paulo from January 2003 to December 2007. Data were analyzed from January 15, 2018, to October 15, 2019. Exposure: Longitudinal HbA1c values. Main Outcomes and Measures: The combined outcome of all-cause mortality, myocardial infarction, and ischemic stroke. Results: Of 888 patients with type 2 diabetes and multivessel CAD, 725 (81.6%; median [range] age, 62.4 [55.7-68.0] years; 467 [64.4%] men) had complete clinical and HbA1c information during a median (interquartile range) follow-up period of 10.0 (8.0-12.3) years, with a mean (SD) of 9.5 (3.8) HbA1c values for each patient. The composite end point of death, myocardial infarction, or ischemic stroke occurred in 262 patients (36.1%). A 1-point increase in the longitudinal value of HbA1c was significantly associated with a 14% higher risk of the combined end point of all-cause mortality, myocardial infarction, and ischemic stroke (hazard ratio, 1.14; 95% CI, 1.04-1.24; P = .002) in the unadjusted analysis. After adjusting for baseline factors (ie, age, sex, 2-vessel or 3-vessel CAD, initial CAD treatments, ejection fraction, and creatinine and low-density lipoprotein cholesterol levels), a 1-point increase in the longitudinal value of HbA1c was associated with a 22% higher risk of the combined end point (hazard ratio, 1.22; 95% CI, 1.12-1.35; P < .001). Conclusions and Relevance: Longitudinal increase of HbA1c was independently associated with higher rates of cardiovascular events in patients with type 2 diabetes and multivessel CAD.

Clinical significance of chronic myocardial ischemia in coronary artery disease patients.

Myocardial ischemia is considered the cornerstone of the treatment of patients with coronary artery disease (CAD). Although the deleterious effects of myocardial infarction, the maximum expression of ischemia, have been extensively studied and described, the clinical effects of chronic, documented myocardial ischemia are not completely clarified. The first studies that compared therapies for coronary disease focused on the presence of anatomical features and assessed ischemia based on the interpretation of the findings of obstructive atherosclerotic lesions. They suggested that revascularization interventions did not confer any clinical advantage over medical therapy (MT), in terms of cardiac or overall death. Other retrospective studies that were dedicated to assessing the impact of documented stress-induced ischemia on cardiovascular outcomes have suggested a prognostic impact of chronic ischemia. However, this has been questioned in recent studies. Moreover, the previous understanding that chronic ischemia could lead to worsening of ventricular function was not confirmed in a recent study. Thus, the prognostic significance of stress-induced ischemia has been questioned. Regarding treatment options, although some previous analyses have suggested that interventional therapies would reduce cardiovascular events in CAD patients with documented ischemia, recent post-hoc studies and metanalysis have shown distinct results. In this review article, the authors discuss myocardial ischemia, the different responses of the myocardium to ischemic insults, ischemic preconditioning, and the main findings of recent studies about the clinical aspects and treatment of patients with chronic, documented myocardial ischemia.