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World Journal of Cardiology Jul 2011We describe a patient with asymptomatic apical hypertrophic cardiomyopathy (AHCM) who later developed cardiac arrhythmias, and briefly discuss the diagnostic modalities,...
We describe a patient with asymptomatic apical hypertrophic cardiomyopathy (AHCM) who later developed cardiac arrhythmias, and briefly discuss the diagnostic modalities, differential diagnosis and treatment option for this condition. AHCM is a rare form of hypertrophic cardiomyopathy which classically involves the apex of the left ventricle. AHCM can be an incidental finding, or patients may present with chest pain, palpitations, dyspnea, syncope, atrial fibrillation, myocardial infarction, embolic events, ventricular fibrillation and congestive heart failure. AHCM is frequently sporadic, but autosomal dominant inheritance has been reported in few families. The most frequent and classic electrocardiogram findings are giant negative T-waves in the precordial leads which are found in the majority of the patients followed by left ventricular (LV) hypertrophy. A transthoracic echocardiogram is the initial diagnostic tool in the evaluation of AHCM and shows hypertrophy of the LV apex. AHCM may mimic other conditions such as LV apical cardiac tumors, LV apical thrombus, isolated ventricular non-compaction, endomyocardial fibrosis and coronary artery disease. Other modalities, including left ventriculography, multislice spiral computed tomography, and cardiac magnetic resonance imagings are also valuable tools and are frequently used to differentiate AHCH from other conditions. Medications used to treat symptomatic patients with AHCM include verapamil, beta-blockers and antiarrhythmic agents such as amiodarone and procainamide. An implantable cardioverter defibrillator is recommended for high risk patients.
PubMed: 21860706
DOI: 10.4330/wjc.v3.i7.256 -
Cells Feb 2019Lupus flares when genetically predisposed people encounter exogenous agents such as infections and sun exposure and drugs such as procainamide and hydralazine, but the... (Review)
Review
Lupus flares when genetically predisposed people encounter exogenous agents such as infections and sun exposure and drugs such as procainamide and hydralazine, but the mechanisms by which these agents trigger the flares has been unclear. Current evidence indicates that procainamide and hydralazine, as well as inflammation caused by the environmental agents, can cause overexpression of genes normally silenced by DNA methylation in CD4⁺ T cells, converting them into autoreactive, proinflammatory cytotoxic cells that are sufficient to cause lupus in mice, and similar cells are found in patients with active lupus. More recent studies demonstrate that these cells comprise a distinct CD4⁺ T cell subset, making it a therapeutic target for the treatment of lupus flares. Transcriptional analyses of this subset reveal proteins uniquely expressed by this subset, which may serve as therapeutic to deplete these cells, treating lupus flares.
Topics: Animals; DNA Methylation; Demethylation; Epigenesis, Genetic; Humans; Lupus Erythematosus, Systemic; T-Lymphocyte Subsets
PubMed: 30764520
DOI: 10.3390/cells8020127 -
Chang Gung Medical Journal Feb 2005A diagnostic triad characterizes Brugada syndrome. It consists of a right bundle branch block, ST-segment elevation in leads V1-V3 and sudden cardiac death (SCD).... (Review)
Review
A diagnostic triad characterizes Brugada syndrome. It consists of a right bundle branch block, ST-segment elevation in leads V1-V3 and sudden cardiac death (SCD). Approximately 50% of patients with Brugada syndrome noted to have familial occurrence, this suggests a genetic component of the disease. Mutations in gene SCN5A, an encoder for human cardiac sodium channel on chromosome 3p21, causes Brugada syndrome. Before considering the diagnosis of Brugada syndrome, exclude precordial ST-segment elevation secondary to acute coronary syndrome, electrolyte imbalance, myocarditis, drug over dosage (cocaine, tricyclic antidepressants), and arrhythmogenic right ventricular cardiomyopathy/dysplasia. Intravenous administration of ajmaline, flecainide, and procainamide may exaggerate the ST-segment elevation, or unmask it when it is initially absent in patients with suspected Brugada syndrome. Programmed electrical stimulation (PES) may help in risk stratification, and in some cases, establish the diagnosis. However, the accuracy of PES in predicting outcome is debatable, especially in patients showing an asymptomatic Brugada ECG, and reporting no family history of SCD. Treatment with an implantable cardioverter-defibrillator (ICD) is the only established effective therapy for the disease. With ICD therapy, the mortality rate at a 10 year follow-up was 0%. Supporting data for long-term pharmacological therapy with quinidine, or isoproterenol for prevention of SCD, in these patients, is uncomplete. Future advances in understanding the molecular mechanisms of Brugada syndrome may provide answers to many of the controversial issues in the management of this disease.
Topics: Bundle-Branch Block; Death, Sudden, Cardiac; Diagnosis, Differential; Electrocardiography; Humans; Syndrome
PubMed: 15880981
DOI: No ID Found -
American Family Physician Nov 2002Pericarditis, or inflammation of the pericardium, is most often caused by viral infection. It can also develop as a result of bacterial or other infection, autoimmune... (Review)
Review
Pericarditis, or inflammation of the pericardium, is most often caused by viral infection. It can also develop as a result of bacterial or other infection, autoimmune disease, renal failure, injury to the mediastinal area, and the effects of certain drugs (notably hydralazine and procainamide). The clinical features of pericarditis depend on its cause, as well as the volume and type of effusion. Patients with uncomplicated pericarditis have pleuritic-type chest pain that radiates to the left shoulder and may be relieved by leaning forward. Chest radiographs, Doppler studies, and laboratory tests confirm the diagnosis and provide information about the degree of effusion. In most patients, pericarditis is mild and resolves spontaneously, although treatment with a nonsteroidal anti-inflammatory drug or a short course of a corticosteroid may be helpful. When a large pericardial effusion is produced, cardiac function may be compromised, and cardiac tamponade can occur. In patients with longstanding inflammation, the pericardium becomes fibrous or calcified, resulting in constriction of the heart. Drainage or surgical intervention may be necessary in patients with complicated pericarditis.
Topics: Algorithms; Anti-Inflammatory Agents, Non-Steroidal; Cardiac Tamponade; Diagnosis, Differential; Electrocardiography; Humans; Pericardiocentesis; Pericarditis
PubMed: 12449268
DOI: No ID Found -
Annals of Pediatric Cardiology 2021Junctional ectopic tachycardia (JET) is more common in its postoperative form. A thorough understanding of its etiology, pathophysiology, and management strategies is... (Review)
Review
Junctional ectopic tachycardia (JET) is more common in its postoperative form. A thorough understanding of its etiology, pathophysiology, and management strategies is essential. Classically, postoperative JET is considered to arise from surgical trauma. Genetic susceptibility and an intrinsic morphologic/functional defect in the conduction system inherent in congenital heart diseases likely play a significant role. The devastating effects on postoperative hemodynamics warrant prompt attention. A multipronged management approach with general measures, pharmacotherapy, and pacing has decreased morbidity and mortality. Amiodarone and procainamide remain the preferred drugs, while ivabradine appears promising. Carefully planned randomized trials can go a long way in developing a systematic management protocol for postoperative JET.
PubMed: 34667411
DOI: 10.4103/apc.apc_35_21 -
BMJ Clinical Evidence Dec 2010Pulseless ventricular tachycardia and ventricular fibrillation are the main causes of sudden cardiac death, but other ventricular tachyarrhythmias can occur without... (Review)
Review
INTRODUCTION
Pulseless ventricular tachycardia and ventricular fibrillation are the main causes of sudden cardiac death, but other ventricular tachyarrhythmias can occur without haemodynamic compromise. Ventricular arrhythmias occur mainly as a result of myocardial ischaemia or cardiomyopathies, so risk factors are those of cardiovascular disease.
METHODS AND OUTCOMES
We conducted a systematic review and aimed to answer the following clinical questions: What are the effects of electrical therapies for out-of-hospital cardiac arrest associated with ventricular tachycardia or ventricular fibrillation? What are the effects of antiarrhythmic drug treatments for use in out-of-hospital cardiac arrest associated with shock-resistant ventricular tachycardia or ventricular fibrillation? What are the effects of treatments for comatose survivors of out-of-hospital cardiac arrest associated with ventricular tachycardia or ventricular fibrillation? We searched: Medline, Embase, The Cochrane Library, and other important databases up to February 2010 (Clinical Evidence reviews are updated periodically, please check our website for the most up-to-date version of this review). We included harms alerts from relevant organisations such as the US Food and Drug Administration (FDA) and the UK Medicines and Healthcare products Regulatory Agency (MHRA).
RESULTS
We found 15 systematic reviews and RCTs that met our inclusion criteria. We performed a GRADE evaluation of the quality of evidence for interventions.
CONCLUSIONS
In this systematic review we present information relating to the effectiveness and safety of the following interventions: amiodarone, bretylium, defibrillation, lidocaine, procainamide, and therapeutic hypothermia.
Topics: Amiodarone; Death, Sudden, Cardiac; Electric Countershock; Humans; Hypothermia, Induced; Lidocaine; Out-of-Hospital Cardiac Arrest; Ventricular Fibrillation
PubMed: 21418694
DOI: No ID Found -
British Journal of Anaesthesia Jul 1979
Review
Topics: Adrenergic beta-Antagonists; Anesthetics; Animals; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Disopyramide; Dogs; Humans; Intraoperative Complications; Lidocaine; Mexiletine; Phenytoin; Procainamide; Succinylcholine
PubMed: 45077
DOI: 10.1093/bja/51.7.659 -
Postgraduate Medical Journal Mar 1972
Review
Topics: Adrenergic beta-Antagonists; Arrhythmias, Cardiac; Digitalis Glycosides; Edetic Acid; Electric Countershock; Electrocardiography; Feeding and Eating Disorders; Heart Block; Heart Failure; Humans; Lactones; Lidocaine; Magnesium; Nausea; Pacemaker, Artificial; Phenytoin; Potassium; Procainamide; Propranolol; Quinidine; Vision Disorders; Vomiting
PubMed: 4401938
DOI: 10.1136/pgmj.48.557.163 -
Clinics and Practice Sep 2011The authors report a case of cardiac arrest in a patient receiving intravenous (IV) metoclopramide and review the pertinent literature. A 62-year-old morbidly obese...
The authors report a case of cardiac arrest in a patient receiving intravenous (IV) metoclopramide and review the pertinent literature. A 62-year-old morbidly obese female admitted for a gastric sleeve procedure, developed cardiac arrest within one minute of receiving metoclopramide 10 mg via slow intravenous (IV) injection. Bradycardia at 4 beats/min immediately appeared, progressing rapidly to asystole. Chest compressions restored vital function. Electrocardiogram (ECG) revealed ST depression indicative of myocardial injury. Following intubation, the patient was transferred to the intensive care unit. Various cardiac dysrrhythmias including supraventricular tachycardia (SVT) associated with hypertension and atrial fibrillation occurred. Following IV esmolol and metoprolol, the patient reverted to normal sinus rhythm. Repeat ECGs revealed ST depression resolution without pre-admission changes. Metoclopramide is a non-specific dopamine receptor antagonist. Seven cases of cardiac arrest and one of sinus arrest with metoclopramide were found in the literature. The metoclopramide prescribing information does not list precautions or adverse drug reactions (ADRs) related to cardiac arrest. The reaction is not dose related but may relate to the IV administration route. Coronary artery disease was the sole risk factor identified. According to Naranjo, the association was possible. Other reports of cardiac arrest, severe bradycardia, and SVT were reviewed. In one case, five separate IV doses of 10 mg metoclopramide were immediately followed by asystole repeatedly. The mechanism(s) underlying metoclopramide's cardiac arrest-inducing effects is unknown. Structural similarities to procainamide may play a role. In view of eight previous cases of cardiac arrest from metoclopramide having been reported, further elucidation of this ADR and patient monitoring is needed. Our report should alert clinicians to monitor patients and remain diligent in surveillance and reporting of bradydysrrhythmias and cardiac arrest in patients receiving metoclopramide.
PubMed: 24765383
DOI: 10.4081/cp.2011.e83 -
The Western Journal of Medicine Jun 1986
Topics: Allopurinol; Anti-Bacterial Agents; Body Temperature Regulation; Drug Hypersensitivity; Fever; Humans; Interleukin-1; Isoniazid; Methyldopa; Phenytoin; Procainamide; Quinidine
PubMed: 3487884
DOI: No ID Found