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Myocarditis
Published in Andreas P. Kalogeropoulos, Hal A. Skopicki, Javed Butler, Heart Failure, 2023
George Lazaros, Emilia Lazarou, Dimitris Tousoulis
An ECG should be obtained in all suspected cases of myocarditis. Although a non-specific tool, the ECG shows pathologic findings in most patients with acute myocarditis.14,15 Most patients present with non-specific repolarization abnormalities. ST-segment elevation may raise differential diagnostic issues with acute myocardial infarction.14 Newly appearing Q waves, abnormal QRS axis, and prolongation beyond 120 ms, a QTc greater than 440 ms, and ventricular ectopy have been associated with adverse outcome and a need for transplantation.41
A lorry driver with chest pain
Published in Tim French, Terry Wardle, The Problem-Based Learning Workbook, 2022
The ST segment on a normal ECG is isoelectric (at the same level as the baseline). Elevation of the ST segment is seen in acute myocardial injury, and the leads in which the elevation occurs indicate the area of the myocardial damage. Therefore, specific ECG patterns occur in MI depending upon which coronary artery is occluded (seeFigure 10.2 for a diagrammatic explanation).
Coronary Artery Disease
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
The diagnosis of acute MI starts with initial and serial ECG. Then, serial measurements of cardiac biomarkers help to identify the subtype of MI that is present, or distinguish between these and unstable angina. Additionally, urgent cardiac catheterization is needed for some patients. An ECG is crucial for diagnosis, and must be done within 10 minutes of the patient’s arrival. An initial ECG usually reveals an ST-segment elevation. If possible, emergency coronary angiography and PCI are performed very soon after the onset of an acute MI.
Refractory cardiogenic shock caused by zinc phosphide toxicity
Published in Baylor University Medical Center Proceedings, 2023
Nitish Mittal, Mohamed Elmassry, Mostafa Abohelwa
Phosphine toxicity can impact the cardiovascular system in varied ways. Circulatory system collapse is frequently observed and leads to refractory hypotension and cardiogenic shock.6 Kalra et al reported in a study of 25 patients that phosphine causes decreased cardiac output, inadequate vasoconstriction, and increased systemic venous pressure.7 Moreover, the histological changes in the cardiac tissue include myocardial edema, fiber fragmentation, vacuolization of myocytes, and focal necrosis in certain cases.8 Interestingly, in some patients, dysrhythmias, such as atrial fibrillation, bundle branch blocks, and other supraventricular tachycardias, are observed after exposure to phosphide.9 In addition, ST-segment changes, similar to myocardial infarction, are observed in some patients. Thus, phosphide impacts the cardiovascular system significantly. Some less common features include hepatotoxicity, intravascular hemolysis with methemoglobinemia, and renal failure.1
Rechallenging nivolumab following immune checkpoint inhibitor–induced pericarditis
Published in Baylor University Medical Center Proceedings, 2023
Mustafa Rami Ali, Omar Jamil Darwish, Laith Alhuneafat, Bayan Nidal Abdallah, Yacob Saleh
A 47-year-old man was diagnosed with de novo RCC of the right kidney metastatic to the lungs and bone. His International Metastatic RCC Database Consortium risk score was 2 (intermediate; <1 year to treat from diagnosis, elevated neutrophil count [8890/mm3]).2 First-line sunitinib was started, and 2 months later he developed extensive right lower limb deep vein thrombosis. His disease remained stable for 9 months until he underwent right renal artery embolization to control for hematuria. A computed tomography (CT) scan showed disease progression, so he was started on second-line nivolumab. Thirty-six days later, he reported progressive pleuritic chest pain and dyspnea for 31 days. An electrocardiogram (ECG) showed ST-segment depression in the lateral leads and diffuse PR depression, troponin was negative, and an echocardiogram showed mild pericardial effusion. A diagnosis of pericarditis was made.
Guanxin V attenuates myocardial ischaemia reperfusion injury through regulating iron homeostasis
Published in Pharmaceutical Biology, 2022
Fuqiong Zhou, Zhengguang Zhang, Meiyuan Wang, Weina Zhu, Jie Ruan, Hongyan Long, Yajie Zhang, Ning Gu
The rat MIRI model was established by left anterior descending coronary artery ligation. Briefly, after anaesthesia, the rats were fixed and plugged into a small animal ventilator. Then the intercostal space between third and fourth rib of the left chest was exposed, and the heart was exposed entirely after tearing the pericardium. Subsequently, the left anterior descending coronary artery was ligated with a 6–0 silk suture at approximately 2 mm below the left atrial appendage. The electrocardiogram was utilized to monitor the ST-segment elevation. After 30 min of ischaemia, the ligature loosened and followed by 2 h of reperfusion. For the Sham group, the rats were subjected to the same surgical procedures without ligating the left anterior descending coronary artery. At the end of the reperfusion, the blood samples were collected from abdominal aorta of experimented rats to separate out serum by centrifugation at 3000 rpm for 10 min at 4 °C. Finally, after euthanized with an overdose of pentobarbital (200 mg/kg, i.p.), the hearts of the rats were harvested for further analysis.