Atrioesophageal Fistula Rates Before and After Adoption of Active Esophageal Cooling During Atrial Fibrillation Ablation.

BACKGROUND: Active esophageal cooling reduces the incidence of endoscopically identified severe esophageal lesions during radiofrequency (RF) catheter ablation of the left atrium for the treatment of atrial fibrillation. A formal analysis of the atrioesophageal fistula (AEF) rate with active esophageal cooling has not previously been performed. OBJECTIVES: The authors aimed to compare AEF rates before and after the adoption of active esophageal cooling. METHODS: This institutional review board (IRB)-approved study was a prospective analysis of retrospective data, designed before collecting and analyzing the real-world data. The number of AEFs occurring in equivalent time frames before and after adoption of cooling using a dedicated esophageal cooling device (ensoETM, Attune Medical) were quantified across 25 prespecified hospital systems. AEF rates were then compared using generalized estimating equations robust to cluster correlation. RESULTS: A total of 14,224 patients received active esophageal cooling during RF ablation across the 25 hospital systems, which included a total of 30 separate hospitals. In the time frames before adoption of active cooling, a total of 10,962 patients received primarily luminal esophageal temperature (LET) monitoring during their RF ablations. In the preadoption cohort, a total of 16 AEFs occurred, for an AEF rate of 0.146%, in line with other published estimates for procedures using LET monitoring. In the postadoption cohort, no AEFs were found in the prespecified sites, yielding an AEF rate of 0% (P < 0.0001). CONCLUSIONS: Adoption of active esophageal cooling during RF ablation of the left atrium for the treatment of atrial fibrillation was associated with a significant reduction in AEF rate.

Risk factors and prevention of dabigatran-related gastrointestinal bleeding in patients with atrial fibrillation.

INTRODUCTION: Dabigatran, as compared with warfarin, was associated with lower rates of stroke and systemic embolism with similar rates of major hemorrhage. But it has a significantly higher risk of gastrointestinal bleeding (GIB). There are limited data on how to prevent GIB from dabigatran and what are the risk factors. METHODS: We performed a retrospective cohort study of patients with atrial fibrillation who have ever taken dabigatran for thromboprophylaxis from October 2010 to February 2013. RESULTS: A total of 247 patients were identified. There were 10 (4%) patients who developed GIB (6 (6.5%) in PPI/H2RA users vs 4 (2.6%) in non-PPI/H2RA users; P = .184). History of GIB within 1 year prior to dabigatran initiation and HAS-BLED score ≥3 are independent risk factors for GIB, with odds ratio of 25.14 (95% CI, 2.85-221.47; P < .01) and 5.85 (95% CI, 1.31-26.15; P = .021), respectively. CONCLUSION: In this real-world cohort, PPI/H2RA use was not associated with reduced GIB events. HAS-BLED score ≥3 and prior history of GIB within 1 year are independent risk factors for GIB among dabigatran users.

Antibiotic-induced cardiac arrhythmias.

This review aims to clarify the underlying risk of arrhythmia associated with the use of macrolides and fluoroquinolones antibiotics. Torsades de pointes (TdP) is a rare potential side effect of fluoroquinolones and macrolide antibiotics. However, the widespread use of these antibiotics compounds the problem. These antibiotics prolong the phase 3 of the action potential and cause early after depolarization and dispersion of repolarization that precipitate TdP. The potency of these drugs, as potassium channel blockers, is very low, and differences between them are minimal. Underlying impaired cardiac repolarization is a prerequisite for arrhythmia induction. Impaired cardiac repolarization can be congenital in the young or acquired in adults. The most important risk factors are a prolonged baseline QTc interval or a combination with class III antiarrhythmic drugs. Modifiable risk factors, including hypokalemia, hypomagnesemia, drug interactions, and bradycardia, should be corrected. In the absence of a major risk factor, the incidence of TdP is very low. The use of these drugs in the appropriate settings of infection should not be altered because of the rare risk of TdP, except among cases with high-risk factors.

Association of high-risk scores for obstructive sleep apnea with symptomatic bradyarrhythmias.

BACKGROUND: Obstructive sleep apnea (OSA) may have an association with bradyarrhythmias but often remains undiagnosed. Our aim was to determine if patients with a high risk of OSA attending our cardiology clinics had an association with symptomatic bradyarrhythmias, as this information might lead to changes in management strategy. METHODS: The Berlin questionnaire was used to assess risk of OSA in 190 patients, and they were divided into high-risk or low-risk groups. Demographic data and medical histories were recorded and patients groups were compared with t-tests and chi-square tests. A multivariate regression analysis was done to correct for confounding variables. RESULTS: The mean age of our sample population was 63.0 ± 14.7 years with a mean BMI of 29.5 ± 7.8 kg/m2. Using the Berlin questionnaire, 41.3% of the patients were classified as high risk; 15.7% of the patients had a known diagnosis of OSA. Between high-risk and low-risk groups, there was no significant difference in the prevalence of bradyarrhythmias (22.5 vs. 15.2% P = 0.21), symptomatic sinus node dysfunction (14.4 vs. 11.4% P = 0.66) or atrioventricular block (10.8 vs. 6.3% P = 0.33). A multivariable logistic regression analysis demonstrated that dyslipidemia had the strongest association with a high risk for OSA, but not bradyarrhythmias. CONCLUSIONS: Based on the Berlin questionnaire, patients at a high risk for OSA did not have an increased prevalence of bradyarrhythmias. More studies are needed to assess the utility of evaluating patients with bradyarrhythmias for OSA prior to implanting permanent pacing devices.

Stand alone surgical ablation for atrial fibrillation.

BACKGROUND: Trials to maintain sinus rhythm in patients with atrial fibrillation (AF) and refractory symptoms have been complicated by lack of success or intolerance of medications. Experience with minimally invasive AF surgery is relatively new, and early results have been promising. However, the study populations and techniques were heterogeneous, and the follow-up periods were short in many series. METHODS: We present a single center experience through a retrospective review of medical records of patients who had minimally invasive AF surgery. RESULTS: The surgical techniques addressed several possible mechanisms of AF and causes of recurrence, including pulmonary vein isolation, underlying substrates modification, ligament of Marshall interruption, ganglion plexus ablation, and left atrial appendage exclusion. Thirty-three cases were identified. The mean duration of follow-up was 23.2 months, and 58.6% were maintained in a sinus rhythm and were off antiarrhythmic drugs at the end of the follow-up period. Cases with persistent AF had a lower success rate. CONCLUSION: Results with minimally invasive surgery are suboptimal at two years of follow-up, particularly for patients with persistent AF.

Atrial fibrillation after inhalational lung injury: a troubling complication of a rare problem.

Atrial fibrillation (AF) has been associated with lung diseases like pneumonia and chronic obstructive pulmonary disease but has only infrequently been associated with inhalational lung injury. We report two cases of resistant AF, which developed in young healthy manual laborers shortly after inhalational lung injury due to massive quantity of pesticides and anhydrous ammonia, respectively. They had no evidence of valvular or structural heart disease and did not have any previous medical problems. The AF was resistant to antiarrhythmic drugs and required pulmonary vein isolation in first patient and possibly the second patient who is currently being evaluated for this procedure. These arrhythmias may reflect direct myocardial injury during and after exposure. Alternatively, multiple mechanisms can cause atrial fibrillation in lung diseases, including hypoxemia, acidemia, inflammatory mediators, and structural changes in the atria and ventricle, and these could lead to AF in inhalational lung injury cases. AF needs to be excluded when patients present with palpitations after inhalational lung injury, especially since, if unrecognized, AF may lead to complications, like thromboembolic phenomenon and tachycardiomyopathy.

Temporary Transvenous Cardiac Pacing in Patients With Acute Myocardial Infarction Predicts Increased Mortality.

BACKGROUND: Temporary pacemakers (TP) are used in emergency situations for severe bradyarrhythmias secondary to acute myocardial infarction (AMI) and to non-AMI related cardiac disorders. TP have been studied previously in AMI patients treated with thrombolytic therapy; limited information is available on current outcomes in AMI patients treated with percutaneous coronary intervention. METHODS: We reviewed the indications, complications, and mortality associated with TP insertion over a four year period (2003 - 2007) at a university hospital. RESULTS: Seventy-three temporary pacemakers were inserted (47 men, 26 women) during this period. The mean age was 65.2 years. TP were used in 29 AMI patients (39.7 % of total) and 44 non-AMI patients (60.3% of total). The duration of TP use was 2.6 ± 0.4 days in the whole cohort, 2.46 % of all AMI patients (29/1180) admitted during this period required a TP. Six of these patients requiring a TP required a permanent pacemaker. Eight patients with AMI and a TP died (27.6%). In contrast 8.9 % of AMI patients not requiring a TP died (P < 0.01). There were no statistically significant differences between the AMI and non-AMI groups in the duration of temporary pacing (2.4 ± 0.6 days vs. 2.8 ± 0.4 days), in complications (27.6% vs. 29.5%), or in mortality (27.6% vs. 15.9%). The need for a permanent pacemaker (PPM) differed significantly between the AMI and non-AMI patients (20.7% vs. 54.5%; P < 0.05). CONCLUSION: Our results indicate that AMI patients infrequently require a TP and that approximately 20% of these patients require a PPM. These results suggest that early revascularization of the conduction system with current interventional techniques has decreased the need for TP in AMI patients. However, this group requires more intensive monitoring as the mortality rate in this group of patients is significantly higher than the other AMI patients not requiring TP.

Effect of pioglitazone on platelet aggregation in a healthy cohort.

BACKGROUND: Peroxisome proliferator-activated receptor (PPAR) agonists can favorably influence atheroma proliferation, lipoprotein metabolism and macrovascular complications. Pioglitazone, one of the thiazolidinedione compounds, is a PPAR ligand activator and a clinically important PPAR agonist. There is controversy in the literature about its potential antiplatelet effects. Its direct platelet inhibition is a novel hypothesis tested in animal models and in human populations with underlying diabetic and/or cardiovascular diseases. The present study was aimed to test the hypothesis of direct platelet aggregation inhibition with the use of pioglitazone in a healthy population. METHODS: This prospective study was started after obtaining institutional review board approval. The platelet aggregation response to adenosine diphosphate, epinephrine, collagen and arachidonic acid was measured in healthy subjects before and after treatment with pioglitazone. The fasting lipid profile including total cholesterol, low-density lipoprotein, very-low-density lipoprotein and high-density lipoprotein was also measured. RESULTS: Twenty subjects, 12 males and 8 females, were enrolled with a mean age of 31.5 ± 7.6 years (range 24-46). Two subjects did not complete the study and were excluded. The mean HbA1C was 5.4% (range 4.7-5.7). The study showed a non-significant platelet aggregation reduction after taking a 7-day pioglitazone course. The adenosine diphosphate-mediated platelet aggregation difference was not significant (p = 0.99); the arachidonic acid-mediated platelet aggregation difference was 0.6% (p = 0.93), for epinephrine 0.9% (p = 0.88) and for collagen 0.2% (p = 0.94). Further, it did not show a favorable response of lipoprotein profile with a non-significant reduction in all lipid panel values even though there is a slight reduction in total cholesterol, triglyceride, low-density lipoprotein and very low-density lipoprotein and a slight increase in high-density lipoprotein. CONCLUSIONS: We conclude that pioglitazone does not have a direct platelet aggregation inhibition effect in a healthy population, nor does it have a favorable effect on lipoprotein profile after a short treatment period.

Prophylactic implantation of cardioverter defibrillators in idiopathic nonischemic cardiomyopathy for the primary prevention of death: a narrative review.

Implantable cardioverter defibrillator (ICD) therapy reduces sudden cardiac death rates and reduces mortality in patients with ischemic heart disease and low ejection fractions. One-third of the deaths in patients with nonischemic cardiomyopathy are sudden. However, the efficacy of ICDs in the primary prevention of death in these patients is less clear. The most common cause of mortality in patients treated with ICDs is heart failure progression. ICD shocks can cause direct myocardial injury, fibrosis, inflammation, and adverse psychological outcomes, and these changes may contribute to the ventricular dysfunction in patients who already have a significantly depressed ejection fraction. We have reviewed the published randomized controlled trials and meta-analysis of prophylactic ICD therapy in the primary prevention of death in patients with nonischemic cardiomyopathy. The individual randomized controlled trials do not report a statistically significant reduction of mortality unless the ICD treatment is added to cardiac resynchronization therapy, but the meta-analysis did show a significant mortality reduction and favored ICD therapy in these patients. Medical management of many study participants was suboptimal, at least based on current guidelines. The patients with non-ischemic cardiomyopathy have good outcomes with medical therapy, and ICD therapy in this relatively low-risk population needs better selection criteria.

Klippel-Trenaunay syndrome and radial artery coronary graft spasm.

A 75-year-old woman with known diagnosis of Klippel-Trenaunay syndrome presented with acute onset of chest pain, dyspnea and elevated cardiac enzymes. She had triple vessel coronary artery disease on subsequent coronary angiography. Given the unavailability of venous conduits secondary to lower extremity varicosities, coronary artery bypass grafting with radial and internal mammary arterial grafts was carried out. The radial artery graft went into spasm two days later and required intracoronary vasodilators to relieve the spasm. The patient remained hypotensive and finally expired.

Implantable cardioverter defibrillators and their role in heart failure progression.

Patients with an implantable cardioverter defibrillator (ICD) implanted for primary prevention have an increased mortality rate if they receive appropriate and/or inappropriate ICD shocks. The most common cause of increased mortality is worsening heart failure. ICD shocks cause direct myocardial injury, contraction band necrosis, and fibrosis, and could induce persistent inflammation. These changes likely contribute to the ventricular dysfunction in patients who have a significantly depressed ejection fraction initially. One-third of the patients with ICDs have psychiatric disorders. Studies have demonstrated that the patients have decreased quality of life, including emotional dysfunction, during the month following an ICD shock. Patients with anxiety and depression have an activated hypothalamus-hypophysis-adrenal axis, increased sympathetic activity, and decreased vagal tone. Chronic sympathetic stimulation could directly affect the myocardium and worsen cardiac dysfunction. Consequently, although ICD implantation is life-saving, it may contribute to heart failure progression. Completed trials need reanalysis to determine whether there are unique characteristics of patients receiving shocks that might lead to additional therapy. Furthermore, the interaction between psychiatric disorders and ICD therapy needs more study.

Transient left ventricular apical ballooning during dobutamine myocardial perfusion imaging.

The transient left ventricular apical ballooning is characterized by wall motion abnormalities involving the apex in the absence of obstructive coronary disease. It is precipitated by acute emotional or physical stress and is most often reported in post-menopausal women. We report a case of transient left ventricular "apical ballooning" without significant coronary artery disease precipitated by high dose dobutamine infusion during pharmacological stress myocardial perfusion imaging. The unique feature of our case was precipitation by chemical stress rather than emotional/physical stress.

Acute cardiac toxicity associated with high-dose intravenous methotrexate therapy: case report and review of the literature.

A 36-year-old woman was hospitalized for preoperative chemotherapy for osteosarcoma. She received intravenous fluids for 12 hours for volume expansion, then methotrexate 24 g (12 g/m2) over 6 hours. This was followed by intravenous leucovorin 200 mg over 1 hour. Two hours after the methotrexate infusion the patient developed chest pain and bradycardia. An electrocardiogram revealed sinus pauses, and telemetry recordings indicated a 4-beat run of ventricular tachycardia. A cardiac work-up consisting of cardiac enzyme level determination, two-dimensional echocardiography, and an adenosine technetium-99m tetrofosmin stress test was negative for structural and ischemic heart disease. The patient recovered without treatment and, approximately 2 weeks later, received a second course of methotrexate at half the dose without complication. One month later the patient received treatment with doxorubicin and cisplatin; 2 days later she died unexpectedly at home. Clinicians should be aware that high-dose methotrexate can cause cardiac symptoms and arrhythmias in previously healthy adults. This complication warrants attention and needs additional clinical investigation.

Deep sternal wound infection caused by group g streptococcus after open-heart surgery.

We report the first case of deep sternal wound infection caused by group G Streptococcus after open-heart surgery. The patient's clinical presentation was nonspecific and his diagnosis was delayed. Surgical debridement and a 4-week course of intravenous antibiotics consisting of sequential penicillin plus gentamicin/ceftriaxone led to recovery. Group G Streptococcus should be suspected as an important postoperative pathogen.

Prognostic value of exercise echocardiography: validation of a new risk index combining echocardiographic, treadmill, and exercise electrocardiographic parameters.

Exercise (Ex) echocardiography has been shown to have significant prognostic power, independent of other known predictors of risk from an Ex stress test. The purpose of this study was to evaluate a risk index, incorporating echocardiographic and conventional Ex variables, for a more comprehensive risk stratification and identification of a very low-risk group. Two consecutive, mutually exclusive populations referred for treadmill Ex echocardiography with the Bruce protocol were investigated: hypothesis-generating (388 patients; 268 males; age 55 +/- 13 years) and hypothesis-testing (105 patients; 61 males age: 54 +/- 14 years).Cardiac events included cardiac death, myocardial infarction, late revascularization (>90 days), hospital admission for unstable angina, and admission for heart failure. Mean follow-up in the hypothesis-generating population was 3.1 years. There were 38 cardiac events. Independent predictors of events by multivariate analysis were: Ex wall motion score index (odds ratio [OR] = 2.77/Unit; P <.001); ischemic S-T depression > or = 1 mm (OR = 2.84; P =.002); and treadmill time (OR = 0.87/min; P =.037). A risk index was generated on the basis of the multivariate Cox regression model as: risk index = 1.02 (Ex wall motion score index) + 1.04 (S-T change) - 0.14 (treadmill time). The validity of this index was tested in the hypothesis-testing population. Event rates at 3 years were lowest (0%) in the lower quartile of risk index (-1.22 to -0.47), highest (29.6%) in the upper quartile (+0.66 to +2.02), and intermediate (19.2% to 15.3%) in the intermediate quartiles. The OR of the risk index for predicting cardiac events was 2.94/Unit ([95% confidence interval: 1.4 to 6.2]; P =.0043). Echocardiographic and Ex parameters are independent powerful predictors of cardiac events after treadmill stress testing. A risk index can be derived with these parameters for a more comprehensive risk stratification with Ex echocardiography.

Molecular remodelling of dystrophin in patients with end-stage cardiomyopathies and reversal in patients on assistance-device therapy.

BACKGROUND: Mutations that lead to disruption of cytoskeletal proteins have been recorded in patients with familial dilated cardiomyopathy. We postulated that changes in cytoskeletal and sarcolemmal proteins provide a final common pathway for dilation and contractile dysfunction in dilated cardiomyopathy. In this study, we investigated the integrity of dystrophin in the myocardium of patients with end-stage heart failure due to ischaemic or dilated cardiomyopathy, and the response to treatment with left-ventricular assistance devices (LVAD). METHODS: We assessed the expression and integrity of dystrophin in myocardial biopsy samples by immunohistochemistry and western-blot analysis using antibodies against the amino-terminal, carboxyl-terminal, and midrod domains. We took samples from the myocardia of ten controls, ten patients with dilated cardiomyopathy, ten with ischaemic heart disease, and six with dilated cardiomyopathy who underwent placement of a left-ventricular assistance device for progressive refractory heart failure. FINDINGS: Immunohistochemical staining identified a disruption to the amino-terminus of dystrophin in 18 of 20 patients with end-stage cardiomyopathy (dilated or ischaemic), whereas staining with antibodies against other domains of dystrophin was normal. Western-blot analysis confirmed these observations, suggesting that remodelling of dystrophin is a common pathway for dysfunction of failing cardiomyocytes. Furthermore, this disruption was reversible in four patients after LVAD support. INTERPRETATION: Dystrophin remodelling is a useful indicator of left-ventricular function in patients with dilated and ischaemic cardiomyopathy. Our results lend support to the hypothesis that changes in cytoskeletal proteins and, in particular, dystrophin might provide a final common pathway for contractile dysfunction in heart failure and these changes might be reversible by reduction of mechanical stress.