Post-prandial premature ventricular contractions provoked by intra-operative jelly drink ingestion: A case report

Reverse Takotsubo Stress Cardiomyopathy During Liver Transplantation

The Premature Ventricular Contraction-Induced Mitral Valvular Cardiomyopathy Successfully Treated by Radiofrequency Ablation: A Case Report

Background: Ventricular arrhythmias (VAs) arising from papillary muscles (PMs) have been reported. Some cases with VAs from PMs have been reported to show late gadolinium enhancement (LGE) in arrhythmogenic PMs on cardiac magnetic resonance imaging (CMRI). Case Report: We report on a 54-year-old female presenting with severe left ventricular dysfunction and frequent premature ventricular contractions (PVCs) including non-sustained ventricular tachycardia (NSVT). PVCs (right bundle branch block and inferior axis) comprised 34.7% of total number of QRS complexes during 24 h Holter monitoring. Three dimensional mapping revealed the origin of PVC at the base of the anterior PM, which was also confirmed by transthoracic echocardiography. A total of 17 radio-frequency (RF) energy applications by irrigated-tip catheter were required to eliminate the PVCs. No Purkinje potential was recorded and acceleration of the PVCs was observed during RF delivery. CMRI revealed LGE in both anterior and posterior PMs. The posterior PM was surrounded by widespread LGE in endocardium while the anterior PM was not. Conclusion: Focal delayed enhancement in the anterior PM may indicate the origin of VAs that can exist deep beneath the endocardium. The posterior PM, which also had LGE in itself was not arrhythmogenic this time possibly because of the widespread LGE covering the area.

Guidewire ablation of epicardial ventricular arrhythmia within the coronary venous system: A case report

A thirty-five-year-old woman without organic heart disease who has exercise-induced ventricular arrhythmias suppressed by propranolol and diltiazem is reported. Treadmill exercise provoked reproducibly nonsustained ventricular tachycardia (NSVT) and salvos of ventricular premature contraction (VPC). QRS morphology of these ventricular arrhythmias showed left bundle branch block pattern and right axis deviation. Oral propranolol (20 mg) and diltiazem (90 mg) prevented exercise provocation of NSVT and VPC. However, oral mexiletine (200 mg) and procainamide (500 mg) could not prevent exercise provocation of these ventricular arrhythmias. No ventricular arrhythmias could be induced by any form of ventricular extrastimulations. Right ventricular pacing at a rate of 210 beats/minute provoked NSVT of which the QRS morphology was similar to that of exercise-induced NSVT. Triggered activity may be a possible electrophysiologic mechanism for exercise-induced ventricular arrhythmias in this patient, although other mechanisms such as reentry and enhanced automaticity could not be completely excluded.

Excerpt It is well known that the electrocardiographic diagnosis of myocardial disease, particularly of myocardial infarction, in the presence of left bundle branch block (LBBB) is difficult. Howev...

Drug-induced disease is a common clinical entity. Drug-inducing anaphylaxis is a serious adverse effect. Several cases of allergic acute coronary syndrome or Kounis syndrome were reported. Premature ventricular contractions are the most frequent cardiac arrhythmia with or without structural heart diseases. A premature ventricular contraction is a sign of decreased oxygenation to the myocardium and anxiety but is also found in a healthy heart. A middle-aged married male patient presented to the physician outpatient clinic with syncope within one hour after ingested one tablet of diclofenac potassium (50mg). Diclofenac potassium-induced anaphylaxis and Kounis type I syndrome with premature ventricular contractions. Electrocardiography, oxygenation, monitoring for vital signs, and echocardiography were the done interventions. The dramatic disappearance of anaphylactic shock, Kounis type I syndrome, coronary artery spasm, and premature ventricular contractions after the traditional treatment of anaphylaxis had happened. Complete clinical and electrocardiographic recovery had achieved. The identi􀏐ication of drug-induced disease is a pivotal step in the diagnosis decision making of any medical problems. Diclofenac potassium can induce anaphylactic shock, Kounis type I syndrome, coronary artery spasm, and premature ventricular contractions. Kounis type I syndrome, coronary artery spasm, and premature ventricular contractions can be reversed with treatment of the cause without using anti-ischemic or ant-arrhythmic measures. Reassurance was the recommended regards diclofenac potassium-induced both coronary artery spasm and premature ventricular contractions that accompanied by anaphylaxis.

The detection of frequent premature ventricular contractions (PVCs) in an athlete represents one of the most important red flags during pre-participation screening. We report the case of a 6-year-old asymptomatic male athlete practicing basketball and sailing, who was examined for pre-participation screening. His resting electrocardiogram showed very frequent, isolated, monomorphic PVCs. The PVCs exhibited a left bundle branch block morphology with an inferior axis and R/S wave precordial transition in lead V3. The most likely origin of PVCs was considered the left ventricular outflow tract. Resting transthoracic echocardiography revealed reduced left ventricular systolic function, with an ejection fraction of 43%, indicating the possible existence of PVC-induced cardiomyopathy. We detected 43,149 isolated monomorphic PVCs (PVC burden: 40%) on 24-h ambulatory electrocardiographic monitoring. Initiation of treatment with atenolol 12.5 mg twice a day led to inadequate reduction of PVCs, with 29,452 isolated monomorphic PVCs (PVC burden: 29%) still observed on 24-h ambulatory electrocardiographic monitoring. After adding flecainide 25 mg twice daily to atenolol treatment, 24-h ambulatory electrocardiographic monitoring revealed complete resolution of ventricular arrhythmias, with no PVCs detected. Left ventricular systolic function recovered to normal. At 12 years of age, the athlete remained on combination therapy with atenolol and flecainide, continued participating in sports, and remained completely asymptomatic with normal cardiac examinations. The optimization of drug treatment was favored over catheter ablation since the athlete was a child and the probable origin of PVCs was the left ventricular outflow tract. This case report highlights that flecainide at a relatively low dose as an add-on therapy to a beta-blocker was highly effective and safe for treating high-burden PVCs originating from the ventricular outflow tract in a juvenile athlete.

Premature ventricular contraction (PVC) is a common type of arrhythmia, and obstructive sleep apnea (OSA) is a common trigger for this condition. Some patients still have PVC, even if ventilation is improved by wearing a respirator. Traditional Chinese medicine (TCM) has a long history of arrhythmia treatment, and this is the first report of a patient with PVC caused by OSA treated with TCM. Twenty-four-hour Holter showed that the number of PVCs decreased from 8968 to 0 before and after TCM treatment, and discomfort symptoms disappeared completely. A 37-year-old middle-aged man, with no history of hypertension, diabetes, hyperlipidemia, or other underlying diseases, had been suffering from OSA for over 1 year and currently uses a respirator to sleep. He was diagnosed with PVC at Beijing Anzhen Hospital 1 year ago and had been taking propafenone hydrochloride tablets following the physician's advice, but palpitation had not been relieved. The patient did not consider surgery and hoped to take TCM to treat the palpitations. The patient was diagnosed with PVC. After excluding other factors that could cause PVC, it was ultimately considered that the patient's PVC was related to OSA. The patient visited Xiyuan Hospital on December 5, 2023, on the basis of existing Western medicine and TCM, using the modified Huanglian Wendan Decoction. After taking TCM for 21 days, the Holter tests were conducted again. The results showed that the number of PVCs decreased from 8968 to 0 within 24 hours. Meanwhile, his palpitations were relieved, and the dosage of propafenone hydrochloride tablets was halved. After 7 days, he did not experience any discomfort; therefore, propafenone hydrochloride tablets were discontinued and TCM was exclusively administered. He received 7 additional courses in TCM. During the final consultation on April 23, 2024, the patient reported no discomfort, and snoring improved. After treatment with TCM, the patient's palpitations disappeared completely and snoring improved, which proved that TCM can treat PVC caused by OSA. To verify this conclusion, more high-quality research is necessary to establish the efficacy and underlying mechanisms of TCM in treating PVC caused by OSA.

Background and Objectives: The effects of gender differences on cardiac parameters have been well-established. In this study, we aimed to evaluate the possible associations of plasma levels of different sex hormones with premature atrial or ventricular contractions in premenopausal women. Materials and Methods: We conducted a prospective study which included women in late reproductive age who presented with palpitations during an eight-month period. A 12-lead electrocardiography, a transthoracic echocardiogram, blood samples, and 24-hour rhythm Holter were conducted on the third day of the menstrual cycle. Results Overall, 93 healthy premenopausal women with a median age of 42 years were enrolled. QTc interval was within normal limits in all patients. The 24 h range of premature atrial contractions (PACs) and premature ventricular contractions (PVCs) was 0–6450 and was 0–21,230, respectively. The median number of PVCs was 540 and the median number of PACs was 212, respectively. In total, 51 patients (54.8%) had a frequency of PVCs > 500/24 h and 37 patients (39.8%) had a frequency of PACs > 500/24 h, respectively. No statistically significant association was shown between any hormone and the frequency of PACs. Regarding PVCs, patients with a PVCs frequency > 500/24 h had higher estradiol levels compared to patients with PVCs less than 500/24 h (median 60 pg/mL versus 42 pg/mL, p = 0.02, OR: 1.01). No association was found between PVCs and other hormones. Conclusions: In premenopausal healthy women, higher estradiol levels are independently associated with increased PVCs. This suggests that estradiol in late reproductive stages may exert proarrhythmic effects.

Mirtazapine, an alpha-2 adrenergic receptor, 5-hydroxytryptamine (5-HT)2, and 5-HT3 antagonist, is commonly used in patients for depression and anorexia. Its mechanism disinhibits serotonin and norepinephrine. Though typically a well-tolerated medication, a rare adverse effect is arrhythmia, including ventricular bigeminy. To date, no case report has cited normal dosing of mirtazapine as a cause of premature ventricular or premature atrial contractions. Only cases of mirtazapine overdose have been associated with arrhythmias, including QT prolongation and bradycardia. We report on a unique case of a 64-year-old female who developed sinus tachycardia with premature ventricular and atrial contractions after starting mirtazapine.

Premature Ventricular Contractions and Atrial Fibrillation: The Reunion of Distant Relatives?

While ventricular premature contractions have been noted during colonoscopy (CS), ventricular fibrillation (VF) is rare. We recently had a patient who developed VF during CS and recovered without any sequelae despite severe complications after cardiopulmonary resuscitation (CPR). If electrocardiogram (ECG) monitoring had been done during CS, a direct current shock defibrillation could have been accomplished and prevented complications. CS in high-risk patients should be done with ECG monitoring.

Dear Editor,We read with great interest the article by Uyanik et al., entitled “Delayed ST-Segment Elevation Due to Electrical Injury Mimicking Acute Myocardial Infarction,” which was published recently in this journal. This case report was mentioning a young patient admitted with late-onset chest pain and ST-segment elevation following ele-ctrical injury (1). Although the case was presented precisely, some points merit further highlighting.Abnormal electrocardiography (ECG) may be found in approxi-mately 31% of patients following an electric shock (2). Non-specific ST-segment changes and sinus tachycardia are the most commonly reported ECG findings; QT prolongation, bundle branch block, atrial and ventricular fibrillation, and atrial and ventricular premature con-tractions are also detected. As referred to in this case report, ST-seg-ment elevation with or without myocardial involvement may follow electrical injury.In a clinical setting, ST-segment elevation on ECG may be related with many conditions, such as myocardial infarction, early repolariza -tion, electrolyte imbalance, and pericarditis. In this case, myocardial infarction may easily be excluded, since cardiac biomarkers are nor-mal and ST elevation is not consistent with myocardial infarction. In this case, ECG shows diffuse and concave ST elevation (elevated at the J point) with the exception of V1 and aVR. In acute myocardial infarction, ST elevation is also accompanied by reciprocal ST depres-sions. In the case of early repolarization, ST elevation is most often present in the mid- to lateral chest leads (V3-V6), and the majority of subjects with early repolarization has no ST deviations in the limb leads. So, early repolarization would be excluded in this patient, who has pronounced ST elevation on D2, D3, and aVF.Zeana describes a 65-year-old electrocuted subject who experi-enced precordial pain, serous enzymes of negative myocardial necro -sis, and ST elevation during 2 weeks of hospitalization (3). These fin-dings suggest the possibility of widespread pericardial involvement. In the case presented by Uyanik et al., pericardial involvement seems to be the most possible cause of ST changes in the admission ECG. This ECG shows us sinus bradycardia with diffuse concave ST elevati-on except for V1 and aVR. ST depression in V1 and aVR is also a typical finding for acute pericarditis. Late-onset chest pain also supports this condition. However, addition of a follow-up ECG of the patient to the report would be more valuable for confirmation of this diagnosis. In our opinion, pericarditis deserves discussion as a possible diagnosis in the aforementioned case.

SCN5A mutation and a short coupled variant of Torsades de Pointes originating from the right ventricle: A case report