Predictors of Trypanosoma cruzi PCR positivity in patients with chronic Chagas disease.

BACKGROUND: A positive Trypanosoma cruzi polymerase chain reaction (PCR) is associated with a worse prognosis in patients with chronic Chagas disease (CD). OBJECTIVES: To study the association of clinical, electrocardiographic, and echocardiographic characteristics and biomarker blood levels with positive T. cruzi PCR in chronic CD. METHODS: This is a single-centre observational cross-sectional study. Positive T. cruzi PCR association with clinical, electrocardiographic, and echocardiographic characteristics, and biomarker blood levels were studied by logistic regression analysis. p values < 0.05 were considered significant. FINDINGS: Among 333 patients with chronic CD (56.4% men; 62 ± 10 years), T. cruzi PCR was positive in 41.1%. Stepwise multivariate logistic regression showed an independent association between positive T. cruzi PCR and diabetes mellitus {odds ratio (OR) 0.53 [95% confidence interval (CI) 0.30-0.93]; p = 0.03}, right bundle branch block [OR 1.78 (95% CI 1.09-2.89); p = 0.02], and history of trypanocidal treatment [OR 0.13 (95% CI 0.04-0.38); p = 0.0002]. Among patients with a history of trypanocidal treatment (n = 39), only four (10%) patients had a positive T. cruzi PCR. MAIN CONCLUSIONS: Among several studied parameters, only diabetes mellitus, right bundle branch block, and history of trypanocidal treatment showed an independent association with positive T. cruzi PCR. History of trypanocidal treatment was a strong protective factor against a positive T. cruzi PCR.

Cardiac Memory: A Case Report and Review of the Literature.

BACKGROUND: A variety of clinical syndromes can cause T-wave inversion (TWI), ranging from life-threatening events to benign conditions. One benign cause of TWI is cardiac memory, which is characterized by the transient inversion of T-waves following abnormal activation of the ventricles, commonly due to intermittent left bundle branch block (LBBB), tachydysrhythmias, electrical pacing, or ventricular pre-excitation. CASE REPORT: A 72-year-old man presented to the emergency department with chest pain, nausea, vomiting, and headache. Upon arrival, his electrocardiogram (ECG) showed new-onset LBBB with appropriate secondary ST-T wave changes. A subsequent ECG showed disappearance of LBBB and newly inverted T-waves in precordial leads V1-V5, followed by a repeat ECG that again showed LBBB. Serial troponin testing was unremarkable. During hospitalization, echocardiogram and nuclear perfusion stress test were normal. The transient TWIs in this patient were believed to be due to cardiac memory. We performed a literature review and identified 39 published cases of cardiac memory. The most common etiology for cardiac memory was after cardiac pacemaker placement, followed by intermittent LBBB (as was seen in our patient), and post-tachydysrhythmia. Patient ages ranged from 21 to 88 years, with an equal number of cases reported in men and women. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Cardiac memory is a poorly understood, rarely observed phenomenon that can occur in the setting of intermittent LBBB. Testing for acute cardiac ischemia and underlying coronary artery disease is still recommended, as the diagnosis of cardiac memory can only be made after negative workup.

From left bundle branch block to Icelandic whales: the multiple perils of atrial fibrillation management in the elderly.

We present the case of an elderly woman which demonstrates how AF therapy in aged individuals is particularly challenging for the presence of complex conditions. The rhythm- or the rate control strategy must be carefully chosen based on individual risk profile. Oral anticoagulant therapy must be wisely managed to maximize benefits-in terms of stroke and dementia control-and to reduce complications.

Ranolazine in treatment of stable angina in woman with atrial fibrillation and intermittent left bundle branch block - a case report.

Stable angina is the most frequent manifestation of ischemic heart disease (IHD) in women as compared to men (65% versus 37%). IHD in women has more favorable clinical course because myocardial infarction develops twice as rare as in men. Coronary angiography of angina patients demonstrates normal coronary arteries more frequently in women than in men. Microvascular angina (MVA) is found to be a rather common form of stable IHD as that particular diagnosis is made later in 20-30% of patients who previously underwent coronary angiography. The disease occurs three times as often in women than in men irrespective of age. Most of these patients are in their perimenopausal age - 45-60 years. The major role in MVA development is considered to be decreased coronary flow reserve resulting from evident endothelial dysfunction of minor coronary arteries. MVA is characterized by great variability of its course and low response to conventional antianginal therapy, particularly in women. In view of this the problem of antianginal drugs which can be used in addition to standard therapy remains to be solved. Ranolazine is a new original antianginal medicine which improves left ventricular diastolic filling by selective inhibition of late Na-flow leading to more effective coronary vessels filling in diastole. The article presents the results of multicenter studies of ranolazine as to its effect on diastolic and systolic functions of the left ventricle, clinical manifestations of angina and heart failure as well as the data on antiarrhythmic action of ranolazine. This article describes the case of successful use of ranolazine as an additional anti-anginal medicine in the 46- year-old female patient diagnosed with microvascular angina. Before taking ranolazine, on the background of conventional treatment of coronary heart disease, the patient developed stable angina and persistent left bundle branch block, atrial fibrillation. After receiving ranolazine, 1000 mg per day for a month, Holter ECG monitoring showed not only significantly reduced number of strokes, the left bundle branch block and atrial fibrillation dissappeared as well. The results indicate a high efficiency of ranolazine as an antianginal, anti-ischemic and anti-arrythmic medicine.

Verapamil-sensitive idiopathic left ventricular tachycardia in a 6-month-old: unique considerations in diagnosis and management in an infant.

Idiopathic left ventricular tachycardia of the Belhassen type is rare in infants. We present a 6-month-old infant girl with a wide-complex tachycardia with right bundle branch block QRS morphology, a superior axis, and atrioventricular dissociation, consistent with a left anterior fascicular tachycardia. Initial echocardiogram revealed depressed ventricular function. The tachycardia was unresponsive to therapeutic trials of adenosine, esmolol, procainamide, and lidocaine. There was brief conversion of the tachycardia to sinus rhythm with transesophageal atrial overdrive pacing, suggesting a reentrant mechanism of the arrhythmia. Ultimately, the judicious administration of intravenous verapamil resulted in termination of the arrhythmia, which has been sustained on oral therapy.

Electrophysiological and haemodynamic effects of vernakalant and flecainide in dyssynchronous canine hearts.

AIMS: About one-third of patients with mild dyssynchronous heart failure suffer from atrial fibrillation (AF). Drugs that convert AF to sinus rhythm may further slowdown ventricular conduction. We aimed to investigate the electrophysiological and haemodynamic effects of vernakalant and flecainide in a canine model of chronic left bundle branch block (LBBB). METHODS AND RESULTS: Left bundle branch block was induced in 12 canines. Four months later, vernakalant or flecainide was administered using a regime, designed to achieve clinically used plasma concentrations of the drugs, n = 6 for each drug. Epicardial electrical contact mapping showed that both drugs uniformly prolonged myocardial conduction time. Vernakalant increased QRS width significantly less than flecainide (17 ± 13 vs. 34 ± 15%, respectively). Nevertheless, both drugs equally decreased LVdP/dtmax by ∼15%, LVdP/dtmin by ∼10%, and left ventricular systolic blood pressure by ∼5% (P = n.s. between drugs). CONCLUSIONS: Vernakalant prolongs ventricular conduction less than flecainide, but both drugs had a similar, moderate negative effect on ventricular contractility and relaxation. Part of these reductions seems to be related to the increase in dyssynchrony.

Chagas disease: don't forget it in Latin American patients with heart block!

Chagas disease is caused by the parasite Trypanosoma cruzi, and mostly affects poor rural populations of central and south America. It is mainly acquired by bugs (triatoma) but also by ingestion of the parasite (fresh fruit juices) or by foetal-maternal blood passing. Despite an important decrease in transmission during the last decades in several countries, millions of patients are still chronically infected and most of them are asymptomatic. In 2012-2013, two cases were admitted in our cardiac intensive care unit (ICU) with heart block due to Chagas cardiomyopathy. Diagnosis was established by echocardiography and positive serological results for Trypanosoma cruzi. This report underlines that in cases of heart failure and conduction abnormalities of unclear aetiology, Chagas disease should be taken into consideration, even in patients originating from non-endemic countries.

Sodium channel blockade with QRS widening after an escitalopram overdose.

INTRODUCTION: Escitalopram is rarely associated with prolongation of the QTc interval; however, there are no reported cases of QRS complex widening associated with escitalopram overdose. We report a case of a patient who presented with both QRS complex widening and QTc interval prolongation after an escitalopram overdose. CASE: A 16-year-old girl presented to the emergency department after ingestion of escitalopram, tramadol/acetaminophen, and hydrocodone/acetaminophen. Laboratory results were significant for 4-hour acetaminophen 21.1 µg/mL. Serum electrolytes including potassium, magnesium, and calcium were all normal. Initial electrocardiogram (ECG) revealed a widened QRS with an incomplete right bundle branch pattern. After administration of 100-mEq sodium bicarbonate, a repeat ECG revealed narrowing of the QRS complex and a prolonged QTc interval. Magnesium sulfate 2 g intravenous and sodium bicarbonate drip were initiated. A repeat ECG, 1 hour after the second, revealed normalization of the QRS complex and QTc interval. DISCUSSION: Prolongation of the QTc interval is an expected effect of escitalopram. Both escitalopram and citalopram are metabolized to the cardiotoxic metabolite S-didesmethylcitalopram and didesmethylcitalopram, respectively, which have been implicated in numerous cardiac abnormalities including widening of the QRS complex. Although never previously described with escitalopram, this mechanism provides a reasonable explanation for the QRS complex widening and incomplete right bundle branch block that occurred in our patient. CONCLUSIONS: Both QRS complex widening and QTc interval prolongation should be monitored in cases of escitalopram and citalopram overdoses.

Recovery of complete left bundle branch block in a dilated cardiomyopathy patient after treatment with sacubitril/valsartan: A case report.

RATIONALE: The treatment of dilated cardiomyopathy (DCM) has recently been greatly improved, especially with the widespread use of sacubitril/valsartan (ARNI) combination therapy. We know that ARNI-like drugs can significantly improve the symptoms of heart failure with reducing ejection fraction. However, clinical studies evaluating the safety and efficacy of ARNI in DCM-associated arrhythmia are limited, and whether individuals with arrhythmia would benefit from ARNI remains controversial. In this case, we report a patient with complete left bundle branch block (CLBBB) associated with DCM whose CLBBB returned to normal after treatment with ARNI. PATIENT CONCERNS: A 38-year-old man was admitted to the hospital for 20 days for idiopathic paroxysmal dyspnea. He presented with exacerbated dyspnea symptoms at night, accompanied by cough and sputum. DIAGNOSIS: Physical examination revealed a grade 4/6 systolic murmur could be heard in the apical area of the heart and mild edema was present in both lower limbs. Laboratory examination found that the B-type natriuretic peptide was significantly increased. Echocardiography indicated left atrial internal diameter, right ventricular internal diameter, and left ventricular diastolic diameter were enlarged and ejection fraction was significantly decreased. Besides, the pulsation of the wall was diffusely attenuated. Electrocardiogram was suggestive of tachycardia and CLBBB. A diagnosis of DCM with CLBBB was considered based on a comprehensive evaluation of the physical examination, laboratory examination, echocardiography and electrocardiogram. INTERVENTIONS: The patient was treated with ARNI at a dose of 50 mg (twice a day) at first, gradually increasing to the target dose (200 mg, twice a day) in the following 9 months as shown in Table 1, along with metoprolol 25 mg (once a day [qd]), diuretics 20 mg (qd), and aldosterone 20 mg (qd). OUTCOMES: After treatment with ARNI during the 9-month follow-up, the patient's symptoms improved, and CLBBB returned to normal. LESSONS: Clinical studies evaluating the safety and efficacy of ARNI in DCM-associated arrhythmia are limited, and whether individuals with arrhythmia would benefit from ARNI remains controversial. This report will help to instruct the clinical treatment of DCM patients with CLBBB and the potential application of ARNI.

Ischemic etiology for adenosine-sensitive fascicular tachycardia.

Adenosine-responsive ventricular tachycardias (VTs) typically occur in patients without structural heart disease; and thus, its association with myocardial ischemia is rare. In this case report, we describe a patient who had demonstrable ischemia along the anterolateral wall of the left ventricle and who developed a VT that was clinically terminated with adenosine. Surface electrocardiogram demonstrated a monomorphic VT with a right bundle-branch block morphology and a rightward axis configuration, and electrophysiologic testing showed atrioventricular dissociation upon atrial pacing and retrograde His waves following induction of VT. These findings localized the patient's VT to the left anterior fascicle, an anatomical region that coincided with the patient's territory of ischemia. We describe the electrophysiologic testing involved in elucidating the patient's tachyarrhythmia, and we provide a brief discussion of the pathogenesis and clinical features of adenosine-sensitive VT. Our case demonstrates that heterogeneous mechanisms of VT are operative in patients with ischemic heart disease.

Amiodarone in patients with left bundle branch block: how to assess the QT interval?

Amiodarone is commonly used for the treatment of supraventricular and ventricular arrhythmias. As a class III antiarrhythmic drug, it prolongs phase III of the cardiac action potential leading to QT interval prolongation. Therefore, the QTc interval should be monitored during amiodarone up-titration to prevent proarrhythmia. However, QTc monitoring in bundle branch block requires some modification as outlined in this case report. The normal upper value of QT interval has been set at 450 ms for males and 460 ms for females. Patients with preexisting bundle branch block (BBB) by definition exhibit wider QRS intervals, ranging between 120 and 200 ms. This 'augmented' QT interval duration is mainly driven by the prolonged time of ventricular depolarization, rather than the time of ventricular repolarization. This inherent QT interval prolongation in BBB can be corrected with specifically designed electrocardiographic formulas. Nevertheless, accurate QT interval calculation at very low or high heart rates remains challenging.

A phenotypic combination of idiopathic VF and Brugada syndrome.

This case study shows a young male presenting a mixture of two disease entities: (1) Brugada syndrome with a nearly-normal baseline electrocardiogram and positive Ajmaline drug challenge as well as (2) idiopathic ventricular fibrillation including extremely short-coupled monomorphic ventricular premature beats (VPB) triggering ventricular fibrillation (coupling interval 318 ± 21 ms). In this phenotypic patient group-more suggestive of idiopathic ventricular fibrillation due to the ultra-short coupling interval of the VPBs-drug treatment with a class IA agent such as Quinidine might be an important option to implantable cardioverter-defibrillator and ablation therapy.

Rare Association of Takotsubo Cardiomyopathy with Right Bundle Branch Block in the Dual Setting of Asthma Exacerbation and Psychiatric Illness.

BACKGROUND Takotsubo cardiomyopathy is characterized by a transient left ventricular dysfunction without obstructive coronary artery disease that mimics an acute myocardial infarction. The electrocardiogram findings of Takotsubo cardiomyopathy usually present with ST-segment elevation or depression, T-wave inversion, left bundle branch block or high-grade atrioventricular block. CASE REPORT This is a report of a case of a 58-year-old male diagnosed with Takotsubo cardiomyopathy that occurred in the setting of an acute asthma exacerbation and psychiatric exacerbation with novel electrocardiogram findings of right bundle branch block. Transthoracic echocardiogram showed a preserved ejection fraction with left ventricular apical ballooning and hyperkinesis of the basal segments. The nuclear stress test showed a fixed perfusion defect at the apical segment, but the patient refused further testing such as coronary angiography. The patient was managed medically, and a repeat echocardiogram done after 8 weeks from discharge showed a complete resolution of the apical ballooning. CONCLUSIONS It is important to recognize that patients with psychiatric illness and asthma exacerbation are predisposed to develop Takotsubo cardiomyopathy. It is also reasonable to suspect Takotsubo cardiomyopathy in the presence of new electrocardiogram findings aside from those typically seen in acute myocardial infarction, especially if it is associated with apical ballooning.

Gemcitabine-induced acute coronary syndrome: a case report.

OBJECTIVES: To report a case of metastatic leiomyosarcoma, in which a patient developed chest pain accompanied by acute left bundle-branch block (LBBB) after gemcitabine infusion. CLINICAL PRESENTATION AND INTERVENTION: A 59-year-old woman admitted with bilateral pulmonary nodules had classic risk factors for coronary heart disease and coronary stenosis as demonstrated by previous coronary angiography. She was treated with gemcitabine infusion, and 30 min later she experienced severe chest pain accompanied by acute LBBB confirmed by ECG. We suspected gemcitabine-induced coronary vasospasm exacerbated by the preexisting coronary artery disease as the cause of the acute coronary syndrome. The patient was subsequently treated with antianginal therapy and percutaneous coronary intervention. Her chest pain resolved and LBBB disappeared. She was discharged 2 days later without any further cardiac events. No additional cancer therapy was given and she died 5 months later, due to disease progression. CONCLUSION: This case showed that chemotherapeutic agents must be administered with intensive cardiac monitoring especially in patients with cardiac disease and well-known risk factors to prevent the development of cardiac complications, despite an agent not being known to be 'cardiotoxic'.

[Intermittent bradycardia-dependent bundle branch block during sevoflurane and remifentanil anesthesia].

Cardiac arrhythmia and bradycardia occasionally occur from the effect of inhaled anesthetic agent and opioid on cardiac conduction. We experienced a case of intermittent bradycardia-dependent bundle branch block (IBDBBB) during sevoflurane and remifentanil anesthesia. A 17-year-old woman suffering from recurrent left ottitis media was scheduled for tympanoplasty under general anesthesia. Her preoperative electrocardiogram (ECG) revealed normal sinus rhythm at heart rate (HR) of 48 beats x min(-1). Her tracheal was intubated following anesthesia induction with propofol and vecuronium, and anesthesia was maintained using inhalation of 40% oxygen with air and 1.5-2.0% sevoflurane, and continuous venous infusion of remifentanil at a rate of 0.15 microg x kg(-1) min(-1). Two hours 20 minutes after starting operation, the P-P interval was constant but the waveforms of low and broad QRS complexes appeared intermittently on the ECG monitor. The blood pressure remained stable at 95/55 mmHg and the HR decreased to 46 beats x min(-1). The waveform of pulse oxymetric oxygen saturation (Spo2) did not change. We diagnosed the ECG pattern as IBDBBB. After intravenous injection of atropine 0.5 mg, the waveforms of QRS complexes recovered to normal sinus rhythm at HR 90 beats x min(-1). Sevoflurane and remifentanil in adolescence could induce ventricular conduction disturbance and result in IBDBBB. Atropine could be effective for IBDBBB induced by sevoflurane and remifentanil.

Combination of cardiac conduction disease and long QT syndrome caused by mutation T1620K in the cardiac sodium channel.

AIMS: The aim of the present study was to elucidate the molecular mechanism underlying the concomitant occurrence of cardiac conduction disease and long QT syndrome (LQT3), two SCN5A channelopathies that are explained by loss-of-function and gain-of-function, respectively, in the cardiac Na+ channel. METHODS AND RESULTS: A Caucasian family with prolonged QT interval, intermittent bundle-branch block, sudden cardiac death, and syncope was investigated. Lidocaine (1 mg/kg i.v.) normalized the prolonged QT interval and rescued bundle-branch block. An SCN5A mutation analysis was performed that revealed a C-to-A mutation at position 4859 (exon 28), predicted to change a highly conserved threonine for a lysine at position 1620. Mutant channels were characterized both in Xenopus oocytes and HEK293 cells. The T1620K mutation remarkably altered the properties of Nav1.5 channels. In particular, the voltage-dependence of the current decay time constants was largely lost. As a consequence, mutant channels inactivated faster than wild-type channels at potentials negative to -30 mV, resulting in less Na+ inward current (loss-of-function), but significantly slower at potentials positive to -30 mV, resulting in an increased Na+ inward current (gain-of-function). Moreover, we found a hyperpolarized shift of steady-state activation and an accelerated recovery from inactivation (gain-of-function). At the same time, channel availability was significantly reduced at the resting membrane potential (loss-of-function). CONCLUSION: We conclude that lysine at position 1620 leads to both loss-of-function and gain-of-function properties in hNav1.5 channels, which may consequently cause in the same individuals impaired impulse propagation in the conduction system and prolonged QTc intervals, respectively.

Case study of thyrotoxic cardiomyopathy.

We present the case of a 65-year-old woman who was referred urgently from primary care with worsening breathlessness for 3 weeks, associated with tachycardia and left bundle branch block (LBBB). She had a background of type 2 diabetes, asthma and hypertension. Initial ECG revealed atrial fibrillation with the fast ventricular rate on the background of LBBB. ECHO findings were consistent with systolic impairment. Initial testing including checking thyroid function test revealed hyperthyroidism. It became evident that this patient had thyrotoxic cardiomyopathy. Early advice from the endocrine team was sought and the patient was treated with a combination of carbimazole and ivabradine. After a hospital stay, she made a remarkable recovery.

Arrhythmias in Severe Trazodone Overdose.

BACKGROUND Trazodone is widely used in the treatment of depression, anxiety, and insomnia. It is thought to have a safe cardiac profile due to the relative lack of anticholinergic effects. Publications about cardiac toxicities of trazodone are scant. CASE REPORT A 55-year-old woman presented with acute disorder of consciousness secondary to an intentional trazodone overdose. She was found to have seizure activity without cerebral edema. The initial electrocardiogram was unremarkable, with a normal QTc interval. She eventually developed QTc prolongation that evolved into ventricular tachycardia, and then into a transient right bundle-branch block, left anterior fascicular block, and variable degrees of atrioventricular nodal blocks at 12-24 h after ingestion. She then developed generalized tonic-clonic seizures, cardiogenic shock, and respiratory arrest. She was intubated and treated with antiepileptics, norepinephrine, and dopamine infusion. QTc interval prolongation gradually resolved and the various forms of heart block did not recur after at 24-36 h. She did not require transcutaneous pacing, and was successfully extubated with intact neurological function. CONCLUSIONS Fatal arrhythmias can occur in trazodone overdose. Close monitoring and supportive care are crucial for patient survival.