ABSTRACT
A 60-year-old man was referred to our hospital presenting with unconsciousness due to severe hyponatremia. The twelvelead ECG on admission exhibited prominent J waves in the inferolateral leads. During the treatment for hyponatremia, ventricular fibrillation (VF) occurred and the electrogram (ECG) after the VF incident exhibited marked ST elevation in the inferolateral leads. An Ach provocation test induced vasospasms in the right and left coronary arteries and J wave augmentation, suggesting a high risk for vasospastic angina. Finally, a subcutaneous implantable cardioverter defibrillator was implanted in the patient. We hereby discuss the possible contribution of hyponatremia to VF episodes in early repolarization syndrome based on the present case.
Subject(s)
Coronary Vasospasm , Electrocardiography , Hyponatremia , Ventricular Fibrillation , Humans , Male , Ventricular Fibrillation/etiology , Ventricular Fibrillation/physiopathology , Ventricular Fibrillation/diagnosis , Middle Aged , Hyponatremia/etiology , Coronary Vasospasm/physiopathology , Coronary Vasospasm/diagnosis , Coronary Vasospasm/complications , Defibrillators, Implantable , SyndromeABSTRACT
Sepsis-induced cardiomyopathy (SICM) is one of the leading indicators for poor prognosis associated with sepsis. Despite its reversibility, prognosis varies widely among patients. Mitochondria play a key role in cellular energy production by generating adenosine triphosphate (ATP), which is vital for myocardial energy metabolism. Over recent years, mounting evidence suggests that severe sepsis not only triggers mitochondrial structural abnormalities such as apoptosis, incomplete autophagy, and mitophagy in cardiomyocytes but also compromises their function, leading to ATP depletion. This metabolic disruption is recognized as a significant contributor to SICM, yet effective treatment options remain elusive. Sepsis cannot be effectively treated with inotropic drugs in failing myocardium due to excessive inflammatory factors that blunt ß-adrenergic receptors. This review will share the recent knowledge on myocardial cell death in sepsis and its molecular mechanisms, focusing on the role of mitochondria as an important metabolic regulator of SICM, and discuss the potential for developing therapies for sepsis-induced myocardial injury.
Subject(s)
Cardiomyopathies , Sepsis , Sepsis/complications , Sepsis/metabolism , Humans , Cardiomyopathies/etiology , Cardiomyopathies/metabolism , Cardiomyopathies/pathology , Animals , Mitochondria, Heart/metabolism , Mitochondria, Heart/pathology , Mitophagy , Energy Metabolism , Mitochondria/metabolism , Mitochondria/pathology , Myocytes, Cardiac/metabolism , Myocytes, Cardiac/pathology , Apoptosis , Adenosine Triphosphate/metabolismABSTRACT
Background: Kounis syndrome (KS) is an underdiagnosed disease. The management of the disease remains elusive because of its infrequency. Case Presentation: A 78-year-old man with anaphylactic shock was admitted to our hospital 2 h after multiple bee stings. After recovering from an anaphylactic reaction, he presented with chest pain with ST elevation. We diagnosed him with KS. After a continuous intravenous infusion of vasodilators, his chest pain and ST elevation improved. However, chest pain with ST-segment elevation recurred the next day. Coronary angiography revealed severe stenosis in the middle left anterior descending coronary artery, and drug-eluting stents were implanted. The patient was discharged on foot after treatment for heart failure. Conclusion: KS, in which anaphylaxis and acute coronary syndrome occur simultaneously, can recur repeatedly after an initial anaphylactic reaction; however, it could be delayed or it could present simultaneously with the anaphylactic reaction. Therefore, long-term observation is important.