1/8. Effect of stress on international normalized ratio during warfarin therapy.OBJECTIVE: To discuss the effect of stress on the international normalized ratio (INR) when patients are taking warfarin. CASE SUMMARY: Two patients at a pharmacist-managed anticoagulation clinic who were stable with anticoagulation developed elevated INR values after a stressful event occurred. All other factors known to elevate the INR were unchanged; furthermore, the INR values returned to the prior level of control after resolution of the stressful events. DISCUSSION: Management of anticoagulation with warfarin requires the knowledge of factors that may alter an INR. Many of these factors, such as dietary changes, illnesses, drug interactions, patient compliance, and physical activity, have been described. In spite of this understanding, many patients continue to experience variability in their INR values, suggesting there are other factors that can alter the INR that have not been fully described. The cases presented here demonstrate that stressful events, physical or psychological, can elevate the INR. The mechanism for this occurrence is unknown, but may be related to decreased metabolism of warfarin during stress. CONCLUSIONS: When an unexplained INR value exists, a stressor should be evaluated as a potential cause.- - - - - - - - - - ranking = 1keywords = physical (Clic here for more details about this article) |
2/8. Pacemaker channel dysfunction in a patient with sinus node disease.The cardiac pacemaker current I(f) is a major determinant of diastolic depolarization in sinus nodal cells and has a key role in heartbeat generation. Therefore, we hypothesized that some forms of "idiopathic" sinus node dysfunction (SND) are related to inherited dysfunctions of cardiac pacemaker ion channels. In a candidate gene approach, a heterozygous 1-bp deletion (1631delC) in exon 5 of the human HCN4 gene was detected in a patient with idiopathic SND. The mutant HCN4 protein (HCN4-573X) had a truncated C-terminus and lacked the cyclic nucleotide-binding domain. COS-7 cells transiently transfected with HCN4-573X cDNA indicated normal intracellular trafficking and membrane integration of HCN4-573X subunits. Patch-clamp experiments showed that HCN4-573X channels mediated I(f)-like currents that were insensitive to increased cellular cAMP levels. Coexpression experiments showed a dominant-negative effect of HCN4-573X subunits on wild-type subunits. These data indicate that the cardiac I(f) channels are functionally expressed but with altered biophysical properties. Taken together, the clinical, genetic, and in vitro data provide a likely explanation for the patient's sinus bradycardia and the chronotropic incompetence.- - - - - - - - - - ranking = 0.5keywords = physical (Clic here for more details about this article) |
3/8. De novo KCNQ1 mutation responsible for atrial fibrillation and short QT syndrome in utero.OBJECTIVE: We describe a genetic basis for atrial fibrillation and short QT syndrome in utero. Heterologous expression of the mutant channel was used to define the physiological consequences of the mutation. methods: A baby girl was born at 38 weeks after induction of delivery that was prompted by bradycardia and irregular rythm. ECG revealed atrial fibrillation with slow ventricular response and short QT interval. Genetic analysis identified a de novo missense mutation in the potassium channel KCNQ1 (V141M). To characterize the physiological consequences of the V141M mutation, xenopus laevis oocytes were injected with cRNA encoding wild-type (wt) KCNQ1 or mutant V141M KCNQ1 subunits, with or without KCNE1. RESULTS: Ionic currents were recorded using standard two-microelectrode voltage clamp techniques. In the absence of KCNE1, wtKCNQ1 and V141M KCNQ1 currents had similar biophysical properties. Coexpression of wtKCNQ1 KCNE1 subunits induced the typical slowly activating and voltage-dependent delayed rectifier K( ) current, I(Ks). In contrast, oocytes injected with cRNA encoding V141M KCNQ1 KCNE1 subunits exhibited an instantaneous and voltage-independent K( )-selective current. Coexpression of V141M and wtKCNQ1 with KCNE1 induced a current with intermediate biophysical properties. Computer modeling showed that the mutation would shorten action potential duration of human ventricular myocytes and abolish pacemaker activity of the sinoatrial node. CONCLUSIONS: The description of a novel, de novo gain of function mutation in KCNQ1, responsible for atrial fibrillation and short QT syndrome in utero indicates that some of these cases may have a genetic basis and confirms a previous hypothesis that gain of function mutations in KCNQ1 channels can shorten the duration of ventricular and atrial action potentials.- - - - - - - - - - ranking = 1keywords = physical (Clic here for more details about this article) |
4/8. Congenital atrial standstill associated with coinheritance of a novel SCN5A mutation and connexin 40 polymorphisms.BACKGROUND: Congenital atrial standstill has been linked to SCN5A. Incomplete penetrance observed in atrial standstill has been attributed in part to the digenic inheritance of polymorphisms in the atrial-specific gap junction connexin 40 (Cx40) in conjunction with an SCN5A mutation. OBJECTIVES: The purpose of this study was to determine the clinical and biophysical characteristics of a novel SCN5A mutation identified in a family with atrial standstill. methods: family members of an apparently sporadic case of atrial standstill underwent genetic screening of SCN5A and atrial-specific genes including Cx40. Biophysical properties of the wild-type (WT) and mutant SCN5A channels in a heterologous expression system were studied using the whole-cell patch clamp technique. RESULTS: The novel SCN5A mutation L212P was identified in the proband (age 11 years) and his father. The father was in normal sinus rhythm. The proband had no P waves on surface ECG, and his right atrium could not be captured by pacing. The recombinant L212P Na channel showed a large hyperpolarizing shift in both the voltage dependence of activation (WT: -48.1 /- 0.9 mV; L212P: -63.5 /- 1.5 mV; P < .001) and inactivation (WT: -86.6 /- 0.9 mV; L212P: -95.6 /- 0.8 mV; P < .001) and delayed recovery from inactivation. Further screenings for genetic variations that might mitigate L212P dysfunction revealed that the proband, but not his father, carries Cx40 polymorphisms inherited from his asymptomatic mother. CONCLUSION: These results suggest that genetic defects in SCN5A most likely underlie atrial standstill. Coinheritance of Cx40 polymorphisms is a possible genetic factor that modifies the clinical manifestation of this inherited arrhythmia.- - - - - - - - - - ranking = 1keywords = physical (Clic here for more details about this article) |
5/8. Acute myocardial infarction in a patient with severe unrecognized mitral stenosis.BACKGROUND: Acute myocardial infarction is a rare complication of mitral stenosis. Acute myocardial infarction in the setting of severe unrecognized mitral stenosis has not been described. CASE REPORT: A 47-year-old-woman was admitted to our department for chest pain typical of myocardial infarction. Electrocardiogram showed ST segment elevation in leads II, III, and aVF and atrial fibrillation. creatine kinase level was elevated to 268 U/L. The diagnosis of acute myocardial infarction of the inferior wall was established. The patient reported breathlessness after physical exertion over the last 2 years; however, she had not sought medical help and was unaware of her heart disease. Transthoracic echocardiography showed severe mitral stenosis (surface mitral valve area <1 cm2) and inferior wall akinesia. CONCLUSIONS: We present a case of acute myocardial infarction in a patient with unrecognized severe mitral stenosis and atrial fibrillation. Our suggestion is that acute myocardial infarction in this patient with no risk factors for coronary atherosclerosis was of thromboembolic origin, from left atrial thrombi.- - - - - - - - - - ranking = 0.5keywords = physical (Clic here for more details about this article) |
6/8. Temporary esophageal stenting allows healing of esophageal perforations following atrial fibrillation ablation procedures.BACKGROUND: Left atrial catheter ablation (LACA) has emerged as a successful method to eliminate atrial fibrillation (AF). Recent reports have described atrio-esophageal fistulas, often resulting in death, from this procedure. Temporary esophageal stenting is an established therapy for malignant esophageal disease. We describe the first case of successful temporary esophageal stenting for an esophageal perforation following LACA. CASE: A 48-year-old man with symptomatic drug refractory lone AF underwent an uneventful LACA. Fifty-nine ablations with an 8-mm tip ablation catheter (30 seconds, 70 Watts, 55 degrees C), as guided by 3-D NavX mapping, were performed in the left atrium to isolate the pulmonary veins as well as a left atrial flutter and roof ablation line. In addition, complex atrial electrograms in AF and sites of vagal innervation were ablated. Two weeks later, he presented with sub-sternal chest pain, fever, and dysphagia. A chest CT showed a 3-mm esophageal perforation at the level of the left atrium with mediastinal soiling and no pericardial effusion. An urgent upper endoscopy with placement of a PolyFlex removable esophageal stent to seal off the esophago-mediastinal fistula was performed. After 3 weeks of i.v. antibiotics, naso-jejunal tube feedings, and esophageal stenting, the perforation resolved and the stent was removed. Over 18 months of follow-up, there have been no other complications, and he has returned to a physically active life and remains free from AF on previously ineffective anti-arrhythmic drugs. CONCLUSION: early diagnosis of esophageal perforations following LACA may allow temporary esophageal stenting with successful esophageal healing. Prompt chest CT scans with oral and i.v. contrast should be considered in any patient with sub-sternal chest pain or dysphagia following LACA.- - - - - - - - - - ranking = 0.5keywords = physical (Clic here for more details about this article) |
7/8. A case of a naval aviator on quinidine for lone atrial fibrillation.While neither atrial fibrillation (AF) nor the therapeutic use of quinidine represent medical contraindications for civil aviation in the united states, they have both been indications for permanent grounding in the U.S. armed forces. We report a case of a naval aviator who was found to be in asymptomatic AF while undergoing a routine annual flight physical. The patient was pharmacologically converted and maintained in normal sinus rhythm with quinidine. Following review of his case by a Special Board of Flight Surgeons, he was returned to limited flight status for dual controlled aircraft only while maintained prophylactically on quinidine to prevent the recurrence of AF.- - - - - - - - - - ranking = 0.5keywords = physical (Clic here for more details about this article) |
8/8. Paroxysmal atrial fibrillation as a cause of potentially lethal ventricular arrhythmia with myocardial ischemia in hypertrophic cardiomyopathy--a case report.The mechanism(s) of myocardial ischemia in hypertrophic cardiomyopathy remain unclear. In this report, the authors present a 75-year-old Japanese woman with nonobstructive hypertrophic cardiomyopathy in whom paroxysmal atrial fibrillation caused severe myocardial ischemia and induced sustained ventricular tachycardia. Her coronary angiogram showed normal findings, and no ischemic changes were provoked by either physical exercise testing or dobutamine stress echocardiography under sinus rhythm. In view of these findings, the rapid ventricular response in the absence of atrial contraction may aggravate or induce myocardial ischemia and predispose patients with hypertrophic cardiomyopathy to develop lethal ventricular arrhythmia.- - - - - - - - - - ranking = 0.5keywords = physical (Clic here for more details about this article) |