Phosphoinositide 3-kinase (PI3K) inhibitors have shown synergistic anticancer effects with endocrine therapy against ER+/PIK3CA-mutated breast cancer. PI3K inhibitors for cancer therapy are becoming more common. There is an increasing need to understand their cardiac adverse events. In this report, we describe the features of near-fatal mixed arrhythmias in a patient who was undergoing a phase Ib clinical study of PI3Kα inhibitor with fulvestrant. Subsequently, the patient survived by cardiopulmonary resuscitation and therefore did not die. This case highlights that PI3K inhibitors can induce QT/QTc prolongation and predispose patients to TdP. The combination of QT/QTc prolongation in combination with prolonged cardiac repolarization, such as an AV block during treatment with PI3Kα inhibitor, may aggravate the occurrence of TdP. It is likely to be a safer strategy to adjust the standard of discontinuing drugs and continuing drugs (QTc interval was <500 and <60 ms at baseline) or choose other types of alternative treatment options. This report provided some ideas for clinicians to identify early and prevent the occurrence of fatal arrhythmias during anticancer treatment.

BACKGROUND: Pulmonary embolisms (PEs) exhibit clinical features similar to those of acute coronary syndrome (ACS), including electrocardiographic abnormalities and elevated troponin levels, which frequently lead to misdiagnoses in emergency situations.
METHODS: Here, we report a case of PE coinciding with chronic coronary syndrome in which the patient\'s condition was obscured by symptoms mimicking ACS. A 68-year-old female with syncope presented to the hospital. Upon admission, she was found to have elevated troponin levels and an electrocardiogram showing ST-segment changes across multiple leads, which initially led to a diagnosis of ACS. Emergency coronary arteriography revealed occlusion of the posterior branches of the left ventricle of the right coronary artery, but based on the complexity of the intervention, the occlusion was considered chronic rather than acute. On the 3rd day after admission, the patient experienced recurrent chest tightness and shortness of breath, which was confirmed as acute PE by emergency computed tomography pulmonary angiography. Following standardized anticoagulation treatment, the patient improved and was subsequently discharged.
CONCLUSIONS: This case report highlights the importance of recognizing the nonspecific features of PE. Clinicians should be vigilant when identifying other clinical features that are difficult to explain accompanying the expected disease, and it is necessary to carefully identify the causes to prevent missed diagnoses or misdiagnoses.

BACKGROUND: Anamorelin, a drug to treat cancer cachexia, binds to ghrelin receptors and improves body weight and appetite. In clinical trials in Japan, patients experienced a 10.7% frequency of stimulant conduction system depression as a severe side effect. Although rare, anamorelin sometimes causes fatal arrhythmias. Because patients with cancer cachexia are often underweight, data on the safety of anamorelin in obese patients are lacking. We report a case of QT interval prolongation after anamorelin administration to an obese patient with non-small cell lung cancer.
METHODS: A female patient with a body mass index of 30 kg/m2 underwent immunotherapy for lung adenocarcinoma. She presented with severe weight loss, anorexia, and fatigue. She had no history of heart disease. On day 12, after administration of anamorelin 100 mg once daily, the patient developed nausea, diarrhea, and anorexia, which were considered cancer immunotherapy-induced immune-related adverse events, and she was admitted to the hospital. An electrocardiogram (ECG) on admission showed a QTc interval of 502 ms. On admission, her hepatic function was Child-Pugh class B, and anamorelin was discontinued the next day. On day 3 after anamorelin discontinuation, the QTc interval was prolonged by up to 557 ms, then decreased to 490 ms on day 6, and improved to 450 ms on day 16. Re-administration of anamorelin was avoided.
CONCLUSIONS: When administering anamorelin to obese patients, we should be aware of the potential for stimulatory conduction system depression, as in underweight patients. Therefore, we should monitor patients by ECG from the early stages of anamorelin administration. Anamorelin is lipophilic, and its volume of distribution is increased in obese patients. Consequently, obese patients may continue to have QT interval prolongation after discontinuation of anamorelin, requiring long-term side-effect monitoring.

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We described an 82-year-old man who was taken to our emergency department after being found unconscious. His electrocardiogram (ECG) showed ST-segment elevation in leads V4-V6 and cardiac troponin I (cTnI) was abnormally elevated. In addition to ECG and cTnI changes, this patient was combined with unconsciousness, high fever, abnormal liver function, acute renal failure, and rhabdomyolysis. The initial diagnosis was heat stroke, so cooling measures were initiated immediately, but a concurrent myocardial infarction was suspected. Meanwhile, emergency coronary angiography was performed, but no severe coronary stenosis or thrombosis was found. We first evaluated quantitative flow ratio (QFR) and coronary angiography-derived index of microvascular resistance (ca-IMR) in patients with heat stroke. Ca-IMR was 260 mmHg*s/m in the left circumflex artery, indicating the presence of coronary microvascular dysfunction (CMD). After several days of treatment, the patient recovered from multiple organ damage. Therefore, ECG and troponin results should be interpreted carefully in patients with high fever and coma during high temperature seasons.

When the electrocardiogram of acute pulmonary embolism is similar to that of acute myocardial infarction, it is difficult to distinguish between the two diseases quickly and effectively. We present the case of a 50-year-old man with acute pulmonary embolism. His electrocardiogram showed subtotal occlusion of the left main coronary artery with ST segment depression in I, II, aVF, V3 to V6, ST segment elevation in aVR, V1 and S1Q3T3. Invasive coronary angiography did not show coronary artery stenosis, then pulmonary angiography was performed quickly which showed massive bilateral acute pulmonary embolism. Electrocardiogram cannot effectively distinguish acute pulmonary embolism from subtotal occlusion of the left main coronary artery. For patients with hemodynamic instability, if ultrasound cannot be performed in time, the combination of invasive coronary angiography and pulmonary angiography can be an option to distinguish acute pulmonary embolism from subtotal occlusion of the left main coronary artery and to treat.

Acute coronary syndrome (ACS) presents significant diagnostic challenges, particularly in cases with atypical presentations and complex clinical scenarios. Here, we describe the case of a 59-year-old man who presented with presyncope, bradycardia, hypotension, and later syncope, attributed to the Bezold-Jarisch reflex. Electrocardiographic findings suggested both inferior and anterior wall infarction, with dynamic changes in T-wave morphology further complicating the diagnostic process. Despite a type A Wellens\' pattern indicating critical stenosis in the proximal left anterior descending (LAD) artery, coronary angiography revealed a complete thrombotic lesion in the proximal right coronary artery (RCA), necessitating urgent intervention. Despite the Wellens pattern indicating LAD involvement, RCA revascularization took precedence due to immediate thrombotic risk. This case underscores the diagnostic challenges associated with conflicting clinical manifestations in ACS and highlights the importance of individualized management strategies integrating advanced diagnostic modalities to optimize outcomes. Understanding the interplay of complex clinical presentations and employing a nuanced approach to management are crucial in effectively navigating ACS scenarios.

Background: Pulmonary embolism (PE) is a common disease with an annual incidence of about 1/1000 persons. About every sixth patient dies within the first 30 days after diagnosis. The electrocardiogram (ECG) is one of the first diagnostic tests performed, and is able to confirm the suspicion of PE with typical electrocardiographic signs. Some ECG signs and their regression are also prognostically relevant. Endovascular mechanical thrombectomy is one option for PE treatment, and aims to relieve right heart strain immediately. The first studies on endovascular mechanical thrombectomy using a dedicated device (FlowTriever System, Inari Medical, Irvine, CA, USA) yielded promising results. Methods: In the following, we report the case of a 66-year-old male patient who presented with New York Heart Association III dyspnea in our emergency department. Among typical clinical and laboratory results, he displayed very impressive electrocardiographic and radiological findings at the time of PE diagnosis. Results: After endovascular mechanical thrombectomy, the patient\'s complaints and pulmonary hemodynamics improved remarkably. In contrast, the ECG worsened paradoxically 18 h after intervention. Nevertheless, control echocardiography 4 days after the intervention no longer showed any signs of right heart strain, and dyspnea had disappeared completely. At a 4-month follow-up visit, the patient presented as completely symptom-free with a high quality of life. His ECG and echocardiography were normal and excluded recurrent right heart strain. Conclusions: Overall, the patient benefitted remarkably from endovascular mechanical thrombectomy, resulting in an almost complete resolution of electrocardiographic PE signs at the 4-month follow-up after exhibiting multiple typical electrocardiographic PE signs at time of diagnosis and initial electrocardiographic worsening 18 h post successful intervention.

Emergency Medicine physicians experience a significant number of interruptions throughout their work day. One common cause of interruptions is the immediate interpretation of triage electrocardiograms (ECGs). Recent studies have suggested that ECGs interpreted as normal via automated analysis by the ECG machine rarely require urgent cardiac intervention and suggested that providers may not have to be interrupted to interpret these \"normal\" ECGs. We describe the case of a patient who presented to the Emergency Department (ED) with chest pain and an ECG interpreted as normal by an automated reading from the ECG machine, despite having acute coronary syndrome requiring emergent intervention.

Drowning is a common cause of childhood morbidity and mortality worldwide. Anoxia, hypothermia, and metabolic acidosis are mainly responsible for this morbidity. Drowning may lead to multiple organ damage, especially cardiac damage, in cases in which severe hypothermia and hypoxemia occur. We report a case of a 4-year-old girl who was admitted to our hospital\'s Emergency Department because of drowning. She had elevated troponin I concentrations and ST-segment elevation with T wave inversion. However, cardiovascular computed tomography showed no obvious abnormalities in the coronary arteries. We suggest that cardiac damage in this situation is caused by coronary artery spasms. To the best of our knowledge, this is the first case of cardiac damage with electrocardiographic changes after drowning in a preschool child.