Alcohol-induced right bundle branch block is associated with a benign outcome in HOCM after alcohol septum ablation (ASA).

INTRODUCTION: Alcohol septum ablation (ASA) is a treatment option for hypertrophic obstructive cardiomyopathy (HOCM). We examined the impact of ASA-induced bundle branch block (BBB) on clinical and hemodynamic features. METHODS AND RESULTS: We retrospectively analysed 98 HOCM patients with regard to ASA-induced BBB. Clinical examination was performed at baseline, early after ASA and at chronic follow-up (FU). ASA reduced left ventricular outflow tract gradient (LVOTG) during chronic FU (69.2 ± 41.6 pre vs. 31.8 ± 30.3 mmHg post ASA; p < 0.05) and interventricular septal diameter (21.7 ± 3.4 pre vs. 18.7 ± 5.0 mm post ASA; p < 0.05). ASA-induced early right BBB (RBBB) until discharge was observed in 44.9% and chronic RBBB at FU in 32.7%. Left BBB (LBBB) occurred in 13.3% early after ASA and in only 4.1% at chronic FU. Chronic RBBB was associated with more pronounced exercise-induced LVOTG reduction (102.1 ± 55.2 with vs. 73.6 ± 60.0 mmHg without; p < 0.05). 6-min-walk-test (6-MWT) and NYHA class were not affected by RBBB. LBBB had no influence on LVOTG, 6-MWT and symptoms. More ethanol was injected in patients with early RBBB (1.1 ± 0.4 vs. 0.8 ± 0.3 ml without; p < 0.05), who also showed higher mean CK release (827 ± 341 vs. 583 ± 279 U/l without; p < 0.05). Pacemaker implantation during FU was necessary in 11.5% of patients with early RBBB, 3.1% with chronic RBBB, 7.7% with early LBBB and 0% with chronic LBBB (p = n.s. for BBB vs. no BBB). CONCLUSION: ASA-induced RBBB is associated with a higher volume of infused ethanol and higher maximum CK release. RBBB does not adversely affect the clinical outcome or need for pacemaker implantation but was associated with higher exercise-induced LVOTG reduction during chronic FU.

Intermittent left bundle branch block and acute heart failure in trastuzumab-induced cardiotoxicity.

A 70-year-old woman with HER2+/ER+ breast cancer on adjuvant trastuzumab therapy without a history of cardiovascular disease presented with respiratory failure from influenza and was found to have intermittent left bundle branch block (LBBB) with new onset systolic heart failure. Her course was complicated by polymorphic ventricular tachycardia and recurrent chest pain. Significant investigations included a normal cardiac MRI and cardiac catheterisation with unobstructed coronaries. It was determined that the aetiology of her heart failure was trastuzumab-induced cardiotoxicity after comprehensive workup. This case highlights an uncommon presentation of LBBB and the steps taken to diagnose a rare cardiomyopathy.

Cocaine-induced pseudo-Wellens' syndrome: a Wellens' phenocopy.

Wellens' syndrome represents critical occlusion of the proximal left anterior descending coronary artery. Electrocardiographic changes similar to Wellens' wave are not exceptional to acute coronary occlusion and can also be seen in cardiac and non-cardiac conditions, such as left ventricular hypertrophy, persistent juvenile T wave, bundle branch blocks, cerebral haemorrhage, pulmonary oedema, pulmonary embolism, pheochromocytoma, Takotsubo syndrome, digitalis and cocaine-induced coronary vasospasm. Cocaine-induced pseudo-Wellens' syndrome should be considered as one of the differentials, since cocaine is used frequently by young adults and can cause left anterior descending coronary vasospasm mimicking Wellens' syndrome. Initiation of the beta-blocking agent in pseudo-Wellens' syndrome as a part of acute coronary syndrome management can be disastrous. We illustrated a case of cocaine-induced pseudo-Wellens' syndrome presented with typical chest pain associated with Wellenoid ECG.

Cytomegalovirus associated severe pneumonia, multi-organ failure and Ganciclovir associated arrhythmia in immunocompetent child.

Cytomegalovirus (CMV) can rarely cause severe manifestations in immunocompetent individuals. Hereby, we report a twelve-year-old boy who presented with tachycardia, tachypnea, fever and leukocytosis, which progressed to hypoxemic respiratory failure and severe acute respiratory distress syndrome (ARDS). Subsequently, he developed multi-organ failure despite the ongoing full supportive care and empiric broad spectrum antibiotics. Cytomegalovirus infection was diagnosed by Polymerase Chain Reaction (PCR) in blood and histopathological examination of lung biopsy. Immunological work up for the child was unremarkable. Ganciclovir therapy was introduced and showed significant improvement until full recovery. However, our patient developed transient heart block as a rare complication for Ganciclovir therapy throughout his course. We present this case with literature review for the CMV infection associated morbidity and mortality among immunocompetent children.

Cardiac arrest in a patient with anterior fascicular block after administration of dexmedetomidine with spinal anesthesia: A case report.

BACKGROUND: Dexmedetomidine is a sedative and analgesic agent that is administered intravenously as an adjunct to spinal anesthesia. It does not suppress the respiratory system significantly, but has adverse effects on the cardiovascular system, for example, bradycardia and hypotension. We here report a patient who underwent cardiac arrest during spinal anesthesia after intravenous infusion of dexmedetomidine. METHODS: A 57-year-old woman with no significant medical history underwent spinal anesthesia for arthroscopic meniscus resection after rupturing the right knee meniscus. Preoperative electrocardiogram revealed sinus bradycardia (54 beats/min) and a left anterior fascicular block. Spinal anesthesia was performed with 11 mg of 0.5% heavy bupivacaine, and the upper level of sensory loss was at T6. Dexmedetomidine infusion was planned at a loading dose of 1.0 mcg kg min over 10 minutes, followed by 0.7 mcg kg min intravenously, as a sedative. Two minutes after dexmedetomidine injection, her heart rate decreased to 31 beats/min and asystole was observed within 10 seconds. RESULTS: After a few minutes of cardiopulmonary resuscitation, spontaneous circulation returned and surgery was completed under general anesthesia. The patient was discharged, and experienced no complications. CONCLUSION: Dexmedetomidine can decrease blood pressure and heart rate, and may cause asystole in some cases. We suggest that dexmedetomidine should be carefully administered under close observation when the parasympathetic nerve system is activated during spinal anesthesia.

[Exercise-induced left bundle branch block with chest pain related to antimalarial prophylaxis with chloroquine]. / Bloc de branche gauche douloureux d'effort associé à la chimioprophylaxie antipaludique par chloroquine.

Left bundle branch block (LBBB) during exercise can be associated with chest pain. Though this association is mostly correlated with an underlying coronary artery disease, painful LBBB has been described in patients with normal coronary arteries. We report a case of exercise-induced LBBB with typical angina pectoris related to antimalarial prophylaxis with chloroquine in a 66-year old woman with normal coronary arteries, which was reversed after treatment discontinuation. The effect of chloroquine on the electrophysiological properties of nodal cardiac tissue is responsible for this rate-dependent LBBB. Precautions for future antimalarial prophylaxis are also discussed.

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.

Arrhythmogenic effect of flecainide toxicity.

Flecainide is a class 1C antiarrhythmic drug especially used for the management of supraventricular arrhythmia. In overdose cases, flecainide can induce life treating ventricular arrhythmias and cardiogenic shock. We report the case of a 72-year-old woman admitted to our intensive care unit for a regular monomorphic wide complex tachycardia (QRS duration 240 ms, right bundle branch block and superior axis morphology) without apparent P waves. Clinical examination showed slight left congestive heart failure signs without cardiogenic shock. An intravenous bolus of 10 mg adenosine 5'-triphosphate (ATP) was ineffective to stop the tachycardia. The diagnosis of ventricular tachycardia induced by flecainide overdose was considered. 500 mL of intravenous 84‰ sodium bicarbonate was administrated. The patient's QRS narrowed immediately and 12-lead ECG showed sinus rhythm. Blood samples confirmed the flecainide overdose and the clinical status progressively improved.

Electrocardiographic findings and cardiac manifestations in acute aluminum phosphide poisoning.

Aluminium phosphide (AlP) poisoning has a high mortality due to cardiovascular involvement. In this study, we evaluated the frequency of cardiac manifestations and electrocardiographic (ECG) findings in 20 patients with acute AlP poisoning, who were admitted to the intensive care unit (ICU) in Tehran, Iran, over a period of 6 months (between October 2008 and April 2009). The sex, age, cause and manner of ingestion, number of ingested AlP tablets, cardiac and ECG manifestations, creatine phosphokinase (CPK), CPK-myocardial band (CPK-mb) and troponin-T (TnT) were extracted from the patients' files. All data were analysed with Statistical Package for the Social Sciences (SPSS) software. The majority (60%) of patients were male. The mean age was 27 ± 8.7 years. The mortality rate was 40%. In all of the patients, the cause of poisoning was intentional suicide and ingestion was the route of exposure. The mean number of ingested AlP tablets per patient was 2.2 ± 1.1. The average time interval between admission and cardiovascular manifestations or ECG findings was 168.8 ± 116.2 min. The range of systolic (SBP) and diastolic blood pressure was 60-130 mmHg and 40-70 mmHg, respectively. Dysrhythmia was observed in nine (45%) cases. Elevation of the ST segment was seen in nine cases (45%). Seven patients (35%) had prolonged QTc intervals. Bundle branch block (BBB) was observed in four (20%) patients. In nine (45%) patients, the serum cardiac TnT qualitative assay was positive. There were no significant differences between normal and abnormal ECG groups according to sex, age, number and manner of ingested AlP tablets and SBP. There was a significant correlation between cardiac manifestations and ECG findings and TnT-positive results with mortality in acute AlP poisoning.

Trastuzumab (Herceptin)-associated cardiomyopathy presented as new onset of complete left bundle-branch block mimicking acute coronary syndrome: a case report and literature review.

Trastuzumab (Herceptin) is well documented in reducing suffering and mortality from breast cancer. The clinically most important side effect of Herceptin is cardiotoxicity, which is reported in 2.6% to 4.5% of patients receiving trastuzumab alone and in as many as 27% of patients when trastuzumab is combined with an anthracycline in metastatic disease. We reported the case of a 50-year-old woman who presented to our emergency department (ED) because of chest pain and shortness of breath. On physical examination, holosystolic murmur over apex could be heard. Pulmonary and abdominal examinations were unremarkable. Twelve-lead electrocardiography showed sinus tachycardia and new onset of complete left bundle-branch block. Emergent transthoracic echocardiography revealed generalized hypokinesia of left ventricle and akinesia over interventricular septum and apex. She subsequently underwent immediate coronary angiography that revealed normal coronary angiography, and left ventriculogram revealed generalized hypokinesia with severe left ventricle dysfunction with ejection fraction of 33%. During right heart catheterization and endomyocardial biopsy, cardiac tamponade developed and was successfully relieved by pericardial window. She was discharged event-free 3 weeks later with conservative treatment. Although new onset of complete left bundle-branch block in a patient with chest pain may be acute coronary syndrome, careful review of medicine history is mandatory to avoid unnecessary procedure and complications.

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'.

Left posterior fascicular block due to high-dose interleukin-2.

OBJECTIVE: To report a case of reversible left posterior fascicular block (LPFB) associated with high-dose interleukin-2 (IL-2) therapy. CASE SUMMARY: A 50-year-old white, nonsmoking male with a history of hypertension, hyperlipidemia, paroxysmal atrial fibrillation, and hypothyroidism had been recently diagnosed with metastatic clear cell-type renal cell carcinoma. He was started on high-dose IL-2 therapy (600,000 IU/kg/dose by 15-min intravenous infusion every 8 h for up to 14 consecutive doses over 5 days, as tolerated). He developed new-onset LPFB after the second dose of IL-2, which was diagnosed electrocardiographically with right axis deviation; deep S waves in lead I; and qR waves in leads II, III, and aVF. He denied chest pain, palpitations, or syncope. The LPFB resolved 18 hours after discontinuation of IL-2 without any potential complications or delay of hospital discharge. The patient completed 9 of 14 doses of IL-2 therapy. Similar electrocardiogram changes were noticed during 2 subsequent cycles of high-dose IL-2 treatment, both of which resolved spontaneously. DISCUSSION: High-dose IL-2 is a Food and Drug Administration-approved biological agent used as monotherapy for the treatment of metastatic renal cell carcinoma and metastatic melanoma. Capillary leak syndrome has been associated with IL-2 therapy and many of its cardiac and noncardiac toxicities. In our patient, LPFB was observed as a reversible adverse reaction to high-dose IL-2 therapy. The Naranjo probability scale indicates a probable relationship between LPFB and high-dose IL-2 in this patient. LPFB has not previously been reported as an adverse reaction associated with high-dose IL-2 therapy. CONCLUSIONS: LPFB may be a reversible cardiac complication associated with high-dose IL-2 therapy. Healthcare professionals should be aware of this potential adverse effect.

Life-threatening adverse drug reaction to paclitaxel. Postmarketing surveillance.

The mechanism of action of hypersensitivity reactions from paclitaxel has not been fully understood. It has not even been defined if they are secondary to paclitaxel, its vehicle or the premedication. Postmarketing pharmacovigilance is predominantly based on spontaneous reporting. These reports albeit biased and incomplete serve to detect previously unrecognised adverse events. We report a life threatening adverse event related to paclitaxel without any evidence of histamine release. It consisted of a cardiac arrest probably secondary to bradiarrhythmia or branch block.

Coronary no-flow and ventricular tachycardia associated with habitual marijuana use.

A 34-year-old man reported heart fluttering and near syncope a few hours after marijuana smoking. In the emergency department, he was found to have a right bundle-branch-type ventricular tachycardia. The patient underwent a successful electric cardioversion. Coronary angiography showed no pericardial artery stenosis yet very slow coronary blood flow. Clinical tachycardia was also inducible in the electrophysiologic laboratory. After verapamil therapy and cessation of marijuana, his coronary flow normalized and ventricular tachycardia was no longer inducible in the electrophysiologic laboratory. Marijuana use might affect coronary microcirculation and cause ventricular tachycardia. Verapamil therapy and cessation of smoking might be curative.

Brugada-type electrocardiographic pattern induced by epidural bupivacaine.

IMPLICATIONS: In this case report, we describe the postoperative occurrence of electrocardiogram changes suggestive for the Brugada syndrome in a patient receiving a continuous epidural bupivacaine infusion. After withdrawal of bupivacaine, the electrocardiogram changes were reversible. The patient's history was unremarkable except for an incomplete right bundle branch block. We conclude that local anesthetics, particularly bupivacaine, have the potential to induce serious arrhythmias in patients with Brugada syndrome.

Vector electrocardiographic alterations after percutaneous septal ablation in obstructive hypertrophic cardiomyopathy. Possible anatomic causes.

OBJECTIVE: Analyze the dromotropic disturbances (vector-electrocardiographic), and the possible anatomic causes, provoked by selective alcohol injection in the septal branch, for percutaneous treatment, of obstructive hypertrophic cardiomyopathy. METHODS: Ten patients with a mean age of 52.7 years underwent percutaneous septal ablation (PTSA) from october 1998; all in functional class III/IV). Twelve-lead electrocardiogram was performed prior to and during PTSA, and later electrocardiogram and vectorcardiogram according to Frank's method. The patients were followed up for 32 months. RESULTS: On electrocardiogram (ECG) prior to PTSA all patients had sinus rhythm and left atrial enlargement, 8 left ventricular hypertrophy of systolic pattern. On ECG immediately after PTSA, 8 had complete right bundle-branch block; 1 transient total atrioventricular block; 1 alternating transient bundle-branch block either right or hemiblock. On late ECG 8 had complete right bundle-branch block confirmed by vectorcardiogram, type 1 or Grishman. CONCLUSION: Septal fibrosis following alcohol injection caused a predominance of complete right bundle-branch block, different from surgery of myotomy/myectomy.