Efficacy and tolerance of high-dose intravenous amiodarone for recurrent, refractory ventricular tachycardia

High-dose intravenous amiodarone was given to 35 patients with recurrent life-threatening ventricular tachycardia (VT) refractory to conventional antiarrhythmic agents. Intravenous amiodarone was given as a 5 mg/kg dose over 30 minutes followed by 20 to 30 mg/kg/day as a constant infusion for 5 days. Twenty-two (63%) patients responded to intravenous amiodarone. All 22 responders received oral amiodarone. Thirteen (59%) continue to receive oral amiodarone after an average follow-up of 19 months, 4 (18%) had sudden cardiac death on oral amiodarone, 2 (9%) died while receiving amiodarone, secondary to left ventricular failure, and 3 (14%) discontinued amiodarone because of side effects. Of the 13 (37%) nonresponders, 10 died in the hospital while receiving intravenous amiodarone, secondary to lethal arrhythmia. Three nonresponders were discharged from the hospital; 2 with automatic cardioverter/defibrillators and 1 receiving a combination of antiarrhythmic agents. Serious adverse events occurred in 13 (37%) patients during intravenous amiodarone therapy. These included hypotension in 8 patients, symptomatic bradycardia in 4 patients and sinus arrest with bradycardia and hypotension in 1 patient. Minor side effects occurred in 23 (66%) patients. In conclusion, high dose intravenous amiodarone is effective in most patients with recurrent, sustained VT but is associated with an unacceptably high incidence of serious adverse events. The optimal dose and duration of intravenous amiodarone for patients with recurrent, refractory sustained VT remain unknown.     

Intravenous Amiodarone

Intravenous amiodarone was approved in 1995 for the treatment of malignant and resistant ventricular arrhythmia. Although it is an “old drug,” much has been learned recently about this complex drug and its application in a variety of cardiac arrhythmias. The objectives of this review were to summarize what is known about intravenous amiodarone, including its pharmacologic and electrophysiologic effects, to review its efficacy for the treatment of patients with highly malignant ventricular arrhythmia and to provide specific information about its clinical use for this and other indications. The studies that were reviewed were selected on the basis of time published (from 1983 to 1995) and the completeness of information provided regarding patient clinical characteristics, drug dosing and methods of evaluation, efficacy analyses, long-term follow-up and complications. The full data from the three controlled trials that formed the basis of the drug’s approval are contained in published reports that were also extensively reviewed. Intravenous amiodarone has demonstrable efficacy for the treatment of frequently recurrent destabilizing ventricular tachycardia and ventricular fibrillation, with suppression rates of 63% to 91% in uncontrolled trials. The three pivotal trials confirmed these findings and demonstrated a dose–response relation, with at least comparable efficacy to bretylium, a drug with a similar indication. The safety profile has also been well described; cardiovascular adverse effects are the most frequent, especially hypotension. Intravenous amiodarone is a useful addition to the drugs available for the treatment of patients with very severe ventricular arrhythmia. Its use in patients with other rhythm disorders appears promising, but final recommendations must await development of definitive data from ongoing clinical trials.(J Am Coll Cardiol 1997;29:1190–8)     

Is it safe to perform cardiac catheterizations on adults with congenital heart disease in a pediatric catheterization laboratory?

OBJECTIVE: To determine the complication rate during the catheterization in adults with congenital heart disease (CHD) in a pediatric catheterization laboratory (PCL). BACKGROUND: An increasing number of patients with CHD are surviving into adulthood, with diagnostic and interventional cardiac catheterization being essential for the management of their disease. The complication rate during the catheterization of adults with CHD has not been reported. METHODS: A retrospective chart review was performed on all adult patients (>18 years) with CHD who underwent diagnostic or interventional catheterization in our PCL within the past 8.5 years. RESULTS: A total of 576 procedures were performed on 436 adult patients (median age 26 years). Complex heart disease was present in 387/576 (67%) procedures. An isolated atrial septal defect or patent foramen ovale was present in 115/576 (20%) procedures, and 51/576 (9%) procedures were performed on patients with structurally normal hearts with arrhythmias. Interventional catheterization was performed in 378/576 (66%) procedures. There were complications during 61/576 (10.6%) procedures; 19 were considered major and 42 minor. Major complications were death (1), ventricular fibrillation (1), hypotension requiring inotropes (7), atrial flutter (3), retroperitoneal hematoma, pneumothorax, hemothorax, aortic dissection, renal failure, myocardial ischemia and stent malposition (1 each). The most common minor complications were vascular entry site hematomas and hypotension not requiring inotropes. Procedures performed on patients > or = 45 years of age had a 19% occurrence of complications overall compared with 9% occurrence rate in patients of age < 45 years (P < 0.01). CONCLUSIONS: The complication rate during the catheterization of adults with CHD in a PCL is similar to the complication rate of children with CHD undergoing cardiac catheterization. The older subset of patients are more likely to encounter complications overall. The encountered complications could be handled effectively in the PCL. With screening in place, it is safe to perform cardiac catheterization on most adults with CHD in a PCL.     

Torsade de pointes caused by high-dose intravenous haloperidol in cardiac patients

Intravenous haloperidol is the agent of choice for controlling severe agitated delirium in seriously ill cardiac patients in many institutions. Prior reports have proposed that high-dose intravenous haloperidol may be without untoward effects in these patients. Recently, however, a few reports of significant QTc prolongation and torsade de pointes as complications of high-dose intravenous haloperidol therapy have appeared. The present report describes three patients with definite haloperidol-induced QTc prolongation and torsade. In each case, QTc prolongation preceded the arrhythmia and disappeared following the discontinuation of haloperidol. Neither electrolyte imbalance, therapy with other cardiac drugs, bradycardia, ischemia, left ventricular dysfunction, nor other known cause of torsade was present in these patients. It is hypothesized that QTc prolongation and torsade likely are idiosyncratic, unpredictable reactions to high-dose haloperidol in select patients. Careful serial electrocardiographic monitoring and prompt discontinuation of the drug should suffice to prevent this relatively uncommon, life-threatening complication of high-dose intravenous haloperidol.     

Coronary artery bypass grafting in the management of ventricular arrhythmias in patients with coronary artery disease

This review analyzes the role of coronary artery bypass grafting in ventricular arrhythmia associated with exertion, problematic sustained ventricular tachycardia, and sudden cardiac death associated with documented ventricular arrhythmia, or first manifestation of coronary artery disease. Specifically discussed is the role of acute ischemia in initiating and perpetuating ventricular arrhythmia. Coronary artery bypass grafting is indicated as a curative intervention for ventricular arrhythmia, but in only one rare instance: exercise-induced ischemia associated with problematic sustained ventricular arrhythmia, when the tachycardia is documented as being induced by acute ischemia. In other instances, indications for coronary artery bypass grafting follow the current guidelines based on clinical trials. Patients with the most severely damaged coronary artery anatomy associated with impaired left ventricular dysfunction have their life expectancy significantly prolonged after coronary artery bypass grafting. These results have been presented as evidence that coronary artery bypass grafting prevents ventricular arrhythmia and sudden cardiac death by modifying the two most powerful predicting factors of sudden cardiac death: coronary artery anatomy and left ventricular function.     

Abrupt Termination of an Ethanol Regimen Provokes Ventricular Arrhythmia and Enhances Susceptibility to the Arrhythmogenic Effects of Epinephrine in Rats

Background: Pathologists examining victims of sudden unexpected death encounter alcoholics more often than expected; alcohol may play a role in sudden arrhythmic death. Here we determine whether a pattern of alcohol consumption, chronic ethanol intake, and withdrawal increases the incidence of malignant ventricular arrhythmia and modulates susceptibility to the arrhythmogenic potential of sympathetic stimulation from an epinephrine test in rats. Methods: Male Wistar rats were treated with a continuous ethanol liquid diet for 7 weeks, and then subjected to 1-day withdrawal or 21-day abstinence. Ventricular ectopy was evaluated by 24-hour electrocardiographic telemetry recording; whole-body sympathetic activation, cardiac sympathovagal balance, and susceptibility to ventricular arrhythmia induced by sympathetic stimulation were evaluated based on blood noradrenalin metabolite concentrations, heart rate variability, and a 3-step epinephrine test. Results: Ventricular arrhythmia and related death were observed only in rats at 1 day of withdrawal, but not in nonalcoholic, continuous ethanol intake or 21-day abstinence rats. One-day withdrawal after a 7-week continuous ethanol regimen elevated circulating noradrenalin metabolite levels and induced cardiac sympathovagal imbalance. Deaths related to the epinephrine test and ventricular arrhythmia induced by low doses of epinephrine were observed only in 1-day withdrawal rats. However, all anomalies were normalized by 21-day abstinence. Conclusions: Abrupt termination of a 7-week continuous ethanol regimen is sufficient to enhance the whole-body sympathetic activation and cardiac sympathovagal imbalance that contribute to ventricular arrhythmia and sudden death in alcoholic rats. Those providing medical care for alcoholics, including in cases of legal imprisonment, should be aware of the possibility of enhanced susceptibility to sudden arrhythmic death due to the abrupt termination of a chronic ethanol regimen.     

Outcomes of cardiac catheterization and percutaneous coronary intervention for in‐hospital ventricular tachycardia or fibrillation cardiac arrest

Objective: This study examined outcomes of patients with sudden cardiac death attributable to primary ventricular tachycardia (VT) or ventricular fibrillation (VF) that underwent cardiac catheterization with or without percutaneous coronary intervention (PCI). Background: The decision to perform cardiac catheterization and PCI in resuscitated patients with sudden cardiac death remains controversial. Prior data suggest a potential benefit from percutaneous revascularization. Methods: All patients with an in‐hospital pulseless VT or VF cardiac arrest from August 2002 to February 2008 who underwent cardiac catheterization were included. Retrospective chart review was performed to obtain clinical, neurologic, and angiographic data. Primary endpoints were all‐cause mortality and neurologic outcome. Results: Two thousand and thirty‐four patients had in‐hospital cardiac arrest, of these 116 had pulseless VT or VF and were resuscitated and 93 (80%) underwent coronary angiography. The median time to follow‐up was 1.3 years (IQR: 0.5–2.9 years). Obstructive coronary artery disease (CAD) was observed in 74 (79%) individuals, of whom 37 underwent PCI. Thirty‐five patients with obstructive CAD (47%) died compared to 41% with nonobstructive CAD. In unadjusted and multivariable adjusted analysis PCI was not associated with lower mortality (adjusted hazard ratio: 1.54, 95% CI, 0.79–3.02, P = 0.20). No significant differences were noted in neurologic status at discharge (P = 0.49). Conclusion: In this study, an aggressive revascularization strategy with PCI did not confer a survival advantage nor was it associated with improved neurologic outcomes. There was no suggestion of harm with PCI and further studies are necessary to identify potential subgroups that may benefit from revascularization. © 2011 Wiley Periodicals, Inc.     

儿茶酚胺敏感性多形性室性心动过速基因特异性管理

儿茶酚胺敏感性多形性室性心动过速(catecholaminergic polymorphic ventricular tachycardia，CPVT)是一种罕见的遗传性疾病，与基因突变导致的心肌细胞内钙稳态的失衡有关，运动或情绪激动可诱发致命性的室性心律失常。CPVT的诊断基于肾上腺素引起的双向性或多形性室性心动过速，部分患者通过基因检测确诊。在治疗上可通过内、外科方法，抑制或阻断肾上腺素对心肌钙稳态的影响。未正规治疗的患者死亡率高，且猝死常为首发症状。文章阐述CPVT的遗传学新发现及其对临床管理的影响，同时阐述基因检测的局限性和级联筛查的最佳应用。     

Acute cardiorespiratory collapse from heparin: a consequence of heparin-induced thrombocytopenia

BACKGROUND: Heparin has rarely been reported to cause acute cardiorespiratory reactions or collapse. Some reports relate this to underlying heparin-induced thrombocytopenia. OBJECTIVE: To confirm and increase awareness of acute life-threatening cardiopulmonary events when patients with heparin-induced thrombocytopenia are re-exposed to heparin. DESIGN: Retrospective observational case series. PATIENTS/SETTING: Four cardiovascular surgery patients were identified in two adjacent large urban hospitals over a 2-yr-period who experienced eight episodes of cardiorespiratory collapse immediately following heparin administration. All had underlying heparin-induced thrombocytopenia. RESULTS: Intravenous boluses of unfractionated heparin were given to four patients with known or previously unrecognized heparin-induced thrombocytopenia. Two patients experienced severe respiratory distress within 15 min for which they required endotracheal intubation. Two other patients experienced cardiac arrest or a lethal arrhythmia within minutes of receiving intravenous heparin. Serologic tests for heparin-induced antibodies were positive in all patients. In three cases, the platelet count was normal or near normal but fell dramatically (71%) immediately following the heparin bolus. Three cases had prior diagnoses of heparin-induced thrombocytopenia, but health care workers administered heparin either unaware of the diagnosis or ignorant of its significance. No patients died, but all required some form of cardiopulmonary resuscitation and subsequent intensive care. CONCLUSIONS: Heparin administration to patients with heparin-induced antibodies can result in life-threatening pulmonary or cardiac events. Appreciation of this phenomenon can unmask cases of heparin-induced thrombocytopenia and strengthens the mandate to avoid any heparin exposure in affected patients. Recognition is crucial to avoiding disastrous outcomes.     

Mitochondrial antioxidant SkQl decreases intensity of ventricular arrhythmias caused by epinephrine

Preventive action of new antioxidant SkQ1 has been studied in rats on model of cardiac arrhythmia caused by epinephrine. The SkQ1 substance was given in dosages from 0.02 up to 20 moles/kg per os 2 weeks prior to experiment. Intravenous bolus introduction of epinephrine (10 or 6 mkg/kg in different experimental series) caused an immediate rise of arterial pressure in average by 19% and decrease in heart rate in average by 44%. The degree of changes of these parameters was approximately identical in all groups. Arrhythmia in the form of ventricular extrasystolia arose in the first 5 min. The total number of extrasystoles, and index of arrhythmia intensity have been 2-3 times lower in rats receiding SkQ1 in doses of 0.5, 2 and 20 moles/kg. It was combined with increased survival rate of animals. Smaller dosages of SkQ1 (0.02-0.1 moles/kg) were ineffective. Results have shown that administration of mitochondrial antioxidant SkQ1 raises stability of the myocardium to arrhythmogenic action of epinephrine.     

Incidence and significance of profound hypotension during dobutamine stress echocardiography

BACKGROUND: Mild hypotension (drops of systolic blood pressure of > or = 20 mmHg) occurs in 14-38% of dobutamine stress echo (DSE) and carries a good prognosis for subsequent cardiac events. The incidence and significance of more profound hypotension (PH) (> or = 50 mmHg) is unknown. HYPOTHESIS: The aim of the study was to determine the incidence of PH during DSE and its prognosis for subsequent cardiac events. METHODS: We reviewed 617 DSE performed at our institution between 1992 and 1996 and identified two DSE subgroups. The first group (PH group) consisted of all patients with PH during DSE. A second group was selected with baseline characteristics similar to the PH group but without PH during DSE (non-PH group). Follow-up was by a physician chart review and direct telephone contact. Cardiac event rates were determined for hard [myocardial infarction (MI), or cardiac death] and soft (angina, congestive heart failure, coronary angioplasty, or coronary bypass surgery) events occurring after the DSE. RESULTS: Of the 617 DSE performed, 16 (3%) patients developed PH (PH group) during DSE, with 13 showing no inducible ischemia. The hard and soft cardiac event rate in this 13 PH group was 46% (mean follow-up of 28.7 +/- 18 months). Of the non-PH group, 32 patients had a negative DSE with a coronary event rate of 12.5%. Profound hypotension correlated with a significantly higher cardiac event rate (p < 0.02). CONCLUSIONS: The incidence of PH during DSE is low (3%) and appears to predict a worse prognosis for subsequent cardiac events.     

Prognostic value of dipyridamole thallium imaging after acute myocardial infarction in older patients

OBJECTIVE: To assess the utility of intravenous dipyridamole thallium testing for predicting major cardiac events following acute myocardial infarction in older patients. DESIGN: Prospective cohort study with a median follow-up of 18 months. SETTING: A university teaching hospital. PARTICIPANTS: 73 patients aged 65 years and older with enzymatically confirmed acute myocardial infarction (mean age 75 years, 56% male, 71% white). MEASUREMENTS: All patients underwent a detailed clinical assessment, an echocardiogram, and an intravenous dipyridamole thallium stress test before hospital discharge. The study endpoint was death or nonfatal reinfarction during the follow-up period. RESULTS: Overall, 24 patients (33%) died or developed recurrent myocardial infarction during follow-up. Among 44 patients with a reversible thallium defect, 19 (43%) reached the study endpoint, compared with only five of 29 patients (17%) without reversible ischemia (P = .04). On multivariate analysis, independent prognostic variables included non-use of aspirin at hospital discharge (P = .002), decreased left ventricular systolic function (P = .009), non-use of a beta-blocker at hospital discharge (P = .013), and reversible ischemia on thallium scintigraphy (P = .025). The relative risks for death or reinfarction associated with non-use of aspirin, non-use of a beta-blocker, left ventricular dysfunction, and reversible ischemia were 2.65, 2.39, 2.01, and 2.51, respectively. Patients with three or four of these risk factors had an 83% probability of death or reinfarction, compared with 41% in patients with two risk factors and 6% in patients with one or no risk factor (P < .001). CONCLUSION: Intravenous dipyridamole thallium imaging provides independent prognostic information in older patients with acute myocardial infarction. Moreover, the combination of clinical, echocardiographic, and dipyridamole thallium variables effectively stratifies older postinfarction patients into high-, intermediate-, and low-risk categories for death or recurrent myocardial infarction.     

Clinical characteristics of hypotension in patients with acute aortic dissection

To evaluate the clinical characteristics, risk factors, and outcomes of hypotension in unselected patients who had acute aortic dissection (AAD), we studied 1,073 such patients who were enrolled in the International Registry of Acute Aortic Dissection between 1996 and 2001. Hypotension was noted in 313 patients (29.2%) who had AAD (46.0% on admission). Multivariate logistic regression identified age >or=70 years (odds ratio [OR] 2.0, 95% confidence interval [CI] 1.4 to 2.9), type A dissection (referent type B AAD; OR 2.1, 95% CI 1.4 to 3.2), neurologic deficit (OR 3.8, 95% CI 2.2 to 6.6), syncope (OR 2.9, 95% CI 1.8 to 4.7), aortic regurgitation requiring valve surgery (OR 1.9, 95% CI 1.1 to 3.3), cardiac tamponade (OR 5.1, 95% CI 3.0 to 8.8), and new Q-wave or ST-segment deviation on an electrocardiogram (OR 1.6, 95% CI 1.1 to 2.4) as independent associations of hypotension (c statistic 0.78). Hospital complications (neurologic deficits 22.7% vs 12.0%, altered mental status 26.1% vs 4.4%, myocardial ischemia 14.6% vs 6.9%, mesenteric ischemia 6.9% vs 2.6%, or limb ischemia 14.6% vs 6.9%, and death 55.0% vs 10.3%) occurred more frequently in patients who had hypotension than in those who did not (p <0.001 for all comparisons). We concluded that hypotension that occurred in >25% of patients who had AAD was associated with a much higher rate of in-hospital adverse events. Our study also identified factors associated with hypotension in patients who had AAD.     

Antiarrhythmic and hemodynamic evaluation of indecainide and procainamide in nonsustained ventricular tachycardia

The present trial was a placebo-controlled, randomized, parallel study comparing indecainide to procainamide. A 24-hour intravenous phase measured and compared invasive hemodynamics, followed by oral administration for assessment of arrhythmia suppression. Thirty-two patients (mean age 61 years) with asymptomatic or mildly symptomatic nonsustained ventricular tachycardia (VT) were evaluated, 15 while receiving indecainide and 17 while receiving procainamide. A total of 8 patients had serious toxicity during the intravenous phase; 6 receiving indecainide experienced increased left ventricular dysfunction or worsening arrhythmia (sustained VT, arrhythmic death) while 2 receiving procainamide developed serious hypotension. Proarrhythmia developed in 3 of 15 (20%) of the indecainide patients, but in no procainamide patient. In those tolerating indecainide, long-term suppression of ventricular premature complexes (VPCs) and of runs of VT was more consistent than with procainamide. While indecainide was a potent suppressor of spontaneous VPCs and VT, patients with significant left ventricular dysfunction could not tolerate it. The indecainide patients developing serious toxicity had a common hemodynamic profile: ejection fraction less than 25%, elevated left ventricular filling pressures, low cardiac and stroke volume index and minimal cardiac reserve. Indecainide has a poor risk-benefit ratio in patients similar to the current population, who have potentially lethal ventricular arrhythmias and severe left ventricular dysfunction.     

Acute myocardial ischemia and ventricular arrhythmias in the pathogenesis of sudden cardiac death in coronary disease

There is increasing evidence for a fatal interaction of myocardial ischemia, ventricular arrhythmias and sudden cardiac death in some patients with coronary artery disease. Evidence comes from autopsy studies, from the evaluation of patients who survived an episode of sudden cardiac death, from follow-up data of these patients either treated or not by revascularization therapy and/or an implantable cardioverter-defibrillator and indicate that reducing the individual ischemic burden will be beneficial to reduce the incidence of sudden cardiac death. Studies in patients with stable and especially with unstable angina using Holter monitoring could demonstrate that there is a close and causal relationship between myocardial ischemia inducing or aggravating life-threatening ventricular arrhythmias and sudden cardiac death particularly in patients with unstable and postinfarction status. This review summarizes some of our clinical knowledge on this topic and indicates that preventive strategies for myocardial ischemia are the antiarrhythmic treatment of choice in patients with severe coronary artery disease and patients with evidence or at risk for ischemic proarrhythmia.     

Efficacy of intracoronary or intravenous VEGF165 in a pig model of chronic myocardial ischemia

OBJECTIVES: We sought to optimize vascular endothelial growth factor (VEGF) treatment for therapeutic angiogenesis in myocardial ischemia, we explored the efficacy of five different regimens. BACKGROUND: Although VEGF165 is one of the most potent pro-angiogenic growth factors, VEGF165 treatment for myocardial ischemia has been hampered by low efficacy and dose-limiting hypotension after systemic or intracoronary delivery. METHODS: This study evaluated the effect of intravenous or intracoronary rhVEGF165 in the presence or absence of nitric oxide (NO) synthase inhibition in a porcine model of chronic myocardial ischemia. Forty-two Yorkshire pigs with chronically occluded left circumflex coronary arteries were randomly assigned to receive 10 microg/kg of VEGF165: 1) rapid (40 min) intravenous VEGF165 0.25 microg/kg/min, 2) slow (200 min) intravenous VEGF165 0.05 microg/kg/min, 3) rapid intracoronary VEGF165 0.25 microg/kg/min, 4) rapid intracoronary VEGF165 0.25 microg/kg/min + nitro-L-arginine methyl ester hydrochloride (L-NAME) or 5) rapid vehicle infusion. RESULTS: Intracoronary and intravenous VEGF165 induced hypotension. Intracoronary VEGF-induced hypotension was blocked by L-NAME. Coronary angiography three weeks after treatment showed improvement in collateral index in both intracoronary groups but not the intravenous VEGF165 groups. Likewise, myocardial blood flow and microvascular function in the ischemic territory improved in both intracoronary groups but not in the intravenous groups. Global and regional myocardial function showed no significant improvements in any groups. CONCLUSIONS: Intracoronary infusion of VEGF165 significantly improves blood flow to the ischemic myocardium. Concomitant administration of L-NAME inhibits VEGF-induced hypotension while most likely preserving VEGF-induced angiogenesis. Intravenous infusion of VEGF165 was not effective in augmenting either myocardial flow or function in this model.     

Short and long QT syndromes: does QT length really matter?

The short and long QT syndromes are inherited diseases associated with an increased risk for life-threatening arrhythmias. The first case of long QT syndrome (LQTS) was reported more than 150 years ago, and the study of this disease led to crucial advancement of our understanding of channelopathies and associated ventricular arrhythmias. Ten years ago, Gussak et al. reported four cases of idiopathic ventricular fibrillation in individuals from a family with a history of sudden cardiac death exhibited very short QT interval and labeled the disease: short QT syndrome (SQTS). Over this decade, the SQTS was found to be a rare inherited syndrome with the potential to provide novel insights into the main mechanisms of cardiac arrhythmogenicity. In this review, we discuss these mechanisms and provocatively question the role of the QT interval duration as a surrogate marker of increased risk for arrhythmia in both the LQTS and the SQTS.     

Drug Therapy For Torsade de Pointes

Torsade de Pointes. Torsade de pointes is an uncommon and unique type of ventricular tachycardia. It differs from other forms of ventricular tachycardia by its morphological features, underlying mechanism, and modes of therapy. Recognizing torsade de pointes is of major clinical importance, as standard antiarrhythmic regimens might not only be ineffective in abolishing this life-threatening arrhythmia but may aggravate it. Torsade de pointes is most commonly precipitated by QT prolonging drugs, mainly type IA antiarrhythmic therapy such as quinidine and disopyramide, and other antiarrhythmic agents are reported to cause torsade de pointes as well. Predisposing factors known to increase the likelihood of developing torsade de pointes are: electrolyte imbalance (hypokalemia, hypomagnesemia, or both) and slow heart rate induced either by sinus bradycardia or heart block. Treatment of torsade de pointes is aimed at shortening the QT interval. By acceleration of the heart rate, the QT interval is shortened, thus preventing the recurrence of the arrhythmia. Treatment of torsade de pointes includes: isoproterenol infusion, cardiac pacing, and intravenous atropine. Intravenous magnesium sulfate, a relatively new mode of therapy for torsade de pointes, was proven to be extremely effective and is now regarded as the treatment of choice for this arrhythmia.( Cardiovasc Electrophysiol, Vol. 4, pp. 206–210, April 1993 )     

Myocardial Injury During Standard Treatment of an Adult with Status Asthmaticus

Asthma affects 5%–10% of adults in the United States. Older adults (> 65 years) with asthma have higher rates of fatal asthma than younger adults. The occurrence of a respiratory emergency, such as status asthmaticus, would seem likely to create a situation of cardiopulmonary dysfunction conducive to myocardial ischemia. However, multiple studies of fatal or near‐fatal asthma have failed to incriminate myocardial infarction as a contributing factor. We report a patient without underlying coronary artery disease who sustained myocardial injury consistent with myocardial ischemia and infarction during status asthmaticus while receiving recommended treatment without intravenous sympathomimetics or theophylline.     

Myocardial injury during standard treatment of an adult with status asthmaticus.

Asthma affects 5%-10% of adults in the United States. Older adults (> 65 years) with asthma have higher rates of fatal asthma than younger adults. The occurrence of a respiratory emergency, such as status asthmaticus, would seem likely to create a situation of cardiopulmonary dysfunction conducive to myocardial ischemia. However, multiple studies of fatal or near-fatal asthma have failed to incriminate myocardial infarction as a contributing factor. We report a patient without underlying coronary artery disease who sustained myocardial injury consistent with myocardial ischemia and infarction during status asthmaticus while receiving recommended treatment without intravenous sympathomimetics or theophylline.