Rare Presentation of Wide QRS Tachycardia in a Patient in Their 40s.

This article describes the case of a 40-year-old individual who presented with fulminant myocarditis. Initial ECG displayed sinus tachycardia with a heart rate of 117 bpm, QS complexes in leads V1-V3, ST-segment depression in leads II, III, aVF, V5-V6, and ST-segment elevation >0.2 mV in leads V1 through V3. The initial clinical assessment suggested an acute anteroseptal myocardial infarction. However, subsequent diagnostic evaluation through coronary angiography disclosed that the coronary arteries were normal. Therefore, clinicians should carefully consider the differential diagnosis between these conditions, as their management strategies differ markedly. Two hours after admission, the patient unexpectedly developed syncope. The ECG findings were consistent with the typical characteristics of bidirectional ventricular tachycardia. Our report described the appearance and morphology as well as mechanism of bidirectional ventricular tachycardia in detail. Additionally, we delineate differential diagnoses for disease that can cause bidirectional ventricular tachycardia, such as aconite poisoning, digoxin overdose, immune checkpoint inhibitor (ICI), myocardial ischemia, and hereditary channelopathies, such as catecholaminergic polymorphic ventricular tachycardia (CPVT) and Andersen-Tawil syndrome. Therefore, clinicians should recognize this ECG finding immediately and initiate appropriate treatment promptly as these measures may be vital in saving the patient's life.

Syncope with QT-interval prolongation and T-wave inversion in anterior and inferior leads: Foreboder of a life-threatening condition?

Even though patients with pulmonary embolism usually present with respiratory distress and tachycardia, the patient presented with syncope only. Typical ECG changes associated with PE include right axis deviation, right bundle-branch block, S1Q3T3 pattern, arrhythmia, nonspecific ST-segment changes, QR pattern in lead V1, Brugada ECG pattern, and T-wave inversions in the precordial leads. However, his electrocardiogram showed QT-interval prolongation and simultaneous T-wave inversions in the inferior and anterior leads. This ECG pattern is crucial for diagnosing PE. The patient underwent computed tomography-pulmonary angiography, which revealed pulmonary embolism. At the same time, these ECG changes should be differentiated from those of long QT syndrome, myocardial ischemia, Takotsubo cardiomyopathy, post-pacing T-wave memory, hypertrophic cardiomyopathy, and subarachnoid hemorrhage.

Arsenic trioxide induces the apoptosis in vascular smooth muscle cells via increasing intracellular calcium and ROS formation.

The present study was designed to investigate whether arsenic trioxide induced the apoptosis in rat mesenteric arterial smooth muscle cells (SMCs), which provides new insights into mechanisms of arsenic-related vascular diseases. Here, we found that arsenic trioxide significantly decreased the viability of SMCs in a dose-dependent manner. In addition, higher level of arsenic trioxide directly caused cellular necrosis. The Hoechst and AO/EB staining demonstrated that apoptotic morphological change was presented in SMCs exposed to arsenic trioxide. The TUNEL assay displayed that more positive apoptotic signal appeared in SMCs treated with arsenic trioxide. The following result showed that ROS formation was markedly increased in arsenic trioxide-treated SMCs. Pretreatment with N-acetylcysteine, an anti-oxidant reagent, obviously attenuated the enhancement of ROS production and the reduction of cell viability induced by arsenic trioxide in SMCs. Arsenic trioxide also enhanced free intracellular Ca(2+) level in SMCs. BAPTA also significantly prevented the increased intracellular Ca(2+) and decreased cell viability induced by arsenic trioxide in SMCs. These results suggested that arsenic trioxide obviously induced apoptosis in SMCs, and its mechanism was partially associated with intracellular ROS formation and free Ca(2+) increasing.

Chest Tightness With QR and ST-Segment Elevation in Lead V1.

This case report describes a patient in their 50s with a 2-month history of worsening chest tightness and dyspnea after COVID-19 infection.

Optimal antithrombotic therapy in patients with atrial fibrillation following percutaneous coronary intervention: A systemic review and meta-analysis.

A challenge for antithrombotic treatment is patients who present with atrial fibrillation (AF) and acute coronary syndrome, particularly in patients who have undergone coronary percutaneous intervention with stenting (PCIS). In the present study, a total of nine observational trials published prior to July 2017 that investigated the effects of dual antiplatelet therapy (DAPT; aspirin + clopidogrel) and triple oral antithrombotic therapy (TOAT; DAPT + warfarin) among patients with AF concurrent to PCIS were collected from the Medline, Cochrane and Embase databases and conference proceedings of cardiology, gastroenterology and neurology meetings. A meta-analysis was performed using fixed- or random-effect models according to heterogeneity. The subgroups were also analyzed on the occurrence of major adverse cardiac events (MACE), stroke and bleeding events in the two treatment groups. Analysis of baseline characteristics indicated that there was no significant difference in the history of coexistent disease or conventional therapies between the DAPT and TOAT groups. The primary end point incidence was 2,588 patients in the DAPT group (n=13,773) and 871 patients in the TOAT group (n=5,262) following pooling of all nine trials. There was no statistically significant difference in the incidence of primary end points between the DAPT and TOAT groups. Odds ratio (OR)=0.96, 95% confidence interval (CI)=0.73-1.27, P=0.79, with heterogeneity between trials (I2=82%, P<0.00001). Subsequently, on subgroup analysis, the results indicated no increased risk of major bleeding or ischemic stroke in the DAPT or TOAT group. However, compared with the TOAT group, there was an apparent increased risk of MACE plus ischemic stroke in the DAPT group (OR=1.62, 95% CI=1.43-1.83, P<0.00001) with heterogeneity between trials (I2=70%, P=0.01). In conclusion, the present meta-analysis suggests that TOAT (aspirin + clopidogrel + warfarin) therapy for patients with AF concurrent to PCIS significantly reduced the risk of MACE and stroke compared with DAPT (aspirin + clopidogrel) therapy. Further randomized controlled clinical trials are required to confirm the efficacy of the optimal antithrombotic therapy in patients with AF following PCIS.

Oral N-acetylcysteine for prophylaxis of contrast-induced nephropathy in patients following coronary angioplasty: A meta-analysis.

It is acknowledged that contrast-induced nephropathy (CIN) is a common cause of acute renal insufficiency after cardiac catheterization and affects mortality and morbidity. To date, it is unknown whether oral N-acetylcysteine (NAC) is able to prevent contrast-induced nephropathy (CIN) in patients undergoing coronary angioplasty. A meta-analysis of randomized controlled trials was performed to assess the effects of NAC in the prevention of CIN in patients following coronary angioplasty. A total of 19 studies published prior to January 2015 that investigated the efficacy of oral NAC for the prevention of CIN were collected from Medline, Cochrane and Embase databases and conference proceedings from cardiology and nephrology meetings. The primary point of investigation was CIN, and the secondary points were renal failure requiring dialysis, mortality and length of hospitalization. The meta-analysis was performed using fixed- or random-effect models according to heterogeneity. Up to January 2015, 19 randomized placebo-controlled clinical trials met the inclusion criteria for the meta-analysis, including 4,514 patients. The pooled data showed that oral NAC did not reduce the CIN incidence [relative risk 0.84, 95% confidence interval (CI) 0.65-1.10; P=0.20], without heterogeneity among trials (I2=29%). Thus, the present meta-analysis suggests that oral NAC therapy is not effective as an alternative treatment to prevent CIN in patients following angioplasty. Further high quality randomized clinical controlled trials are required to confirm the usage and availability of this treatment.