Deepika Misra

Acute pulmonary edema after cardioversion of cardiac arrhythmias

OBJECTIVE To examine the occurrence of acute pulmonary edema after cardioversion of arrhythmias. METHODS Cases, case series, and related articles on the subject identified through a comprehensive literature search were examined. RESULTS Thirty cases (23 males) of post cardioversion acute pulmonary edema were identified. The mean age was 53.8 +/- 13 years (range, 18 to 75 years). Underlying arrhythmias were atrial fibrillation (69%), atrial flutter (24%), supraventricular tachycardia (4%), and ventricular tachycardia (4%). The duration of arrhythmia preceding cardioversion varied widely ranging from 1 day to 13 years. Twenty-six (87%) patients had concomitant cardiovascular disease comprising of coronary artery disease (38%), rheumatic heart disease (23%), cardiomyopathy (23%), and hypertension (8%). Direct current electrical cardioversion was used in 28 (93%) patients and pacing in two (7%) patients. Occurrence of pulmonary edema was independent of the amount of energy used for cardioversion (range 20 to 1280 Joules, mean 263 +/- 27 Joules). Short acting general anesthetic drugs were administered in 14 (47%) and sedation in eight (27%) patients. Sinus rhythm was established in 23 (77%) patients. Duration to develop pulmonary edema after cardioversion was available in 23 patients and ranged from immediately to 96 h. Pulmonary edema occurred within 15 min after cardioversion in 22%, within 3 h in 30%, within 24 h in 30%, within 48 h in 17% and within 96 h in remaining 4% of patients. Three patients required mechanical ventilation. CONCLUSION The rare complication of acute pulmonary edema after cardioversion has been reported mostly in patients with underlying cardiac disease, and is independent of the amount of energy used for cardioversion.

Acute pulmonary edema after successful electrical cardioversion of atrial fibrillation.

Acute pulmonary edema is a rarely reported complication of electrical cardioversion. Most of such cases have been reported after cardioversion of atrial fibrillation. Most of the patients who have been reported to develop postcardioversion acute pulmonary edema had hypertensive or valvular heart disease. We report a case of postcardioversion acute pulmonary edema after electrical cardioversion of atrial fibrillation in a patient with severe mitral regurgitation.

Adenosine induced monomorphic ventricular tachycardia.

Polymorphic ventricular tachycardia has been reported following the administration of adenosine for the treatment of SVT. We present a case of monomorphic ventricular tachycardia in a 75‐year‐old man following the intravenous administration of adenosine for stress testing.

Exercise-induced pulmonary hypertension by stress echocardiography: Prevalence and correlation with right heart hemodynamics

OBJECTIVES The aim of this study was to determine the prevalence of exercise-induced pulmonary hypertension (EIPH) in consecutive subjects referred for stress echocardiography for chest pain or shortness of breath and correlate echocardiographic diagnosis of EIPH with hemodynamics at right heart catheterization (RHC). BACKGROUND Elevated pulmonary pressure can lead to significant morbidity and mortality. EIPH by ehocardiography has been described in patients with connective tissue disease. Its prevalence in the setting of routine clinically indicated stress echocardiography unknown. METHODS In a retrospective analysis of 4068 consecutive stress subjects undergoing stress echocardiography, 479 subjects with EIPH were identified. All 479 subjects with EIPH were compared to 479 age and sex matched subjects with normal pulmonary artery pressures post exercise. EIPH was defined as PASP>50mmHg or peak tricuspid regurgitation velocity>3.2m/s. Of 100 patients with EIPH who underwent RHC we identified variables which predicted abnormal hemodynamic findings on RHC. RESULTS The prevalence of EIPH in subjects referred for stress echocardiography was 11.7%. A greater proportion of subjects with EIPH were obese or had lung disease or connective tissue disease. Of 100 subjects who underwent RHC, 65 had abnormal results. Age>55years (OR 5.1, p<0.01]) or dilated left atrium (OR 4.4, p=0.02]) were independently associated with abnormal right heart hemodynamics. CONCLUSIONS The results demonstrate that 11.7% of patients undergoing clinically indicated stress echocardiography have EIPH. Of those who underwent RHC abnormal hemodynamics were significantly associated with a dilated left atrium or age older than 55years.

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.

EMERGENCY ROOM EVALUATION OF PATIENTS WITH CARDIAC COMPLAINTS AND NEW LEFT BUNDLE BRANCH BLOCK: THE UTILITY OF THE SGARBOSSA AND MODIFIED SGARBOSSA CRITERIA

Background: Accurate recognition of ST elevation myocardial infarction (STEMI) in the presence of left bundle branch block (LBBB) remains a challenge. Sgarbossa criteria has a sensitivity of 52% and a specificity of 98%, while modified Sgarbossa criteria has a sensitivity of 91% and specificity of

A reminder of Escherichia coli sepsis-induced reversible cardiomyopathy

Cardiomyopathy is a progressive disease of myocardium causing either mechanical or electrical disturbances. Sepsis-induced cardiomyopathy (SICM) is an entity of cardiomyopathy which is reversible in 1–2 weeks after recovery from sepsis or septic shock. SICM is thought to have unpredictable cumulative mortality towards sepsis but its exact mechanism remains elusive. We report a case of Escherichia coli SICM in a 63-year-old woman presented with sudden onset of dyspnoea on exertion and orthopnoea following nausea, vomiting and diarrhoea after consuming Chinese foods. Transthoracic echocardiogram revealed severely reduced global left ventricular ejection fraction (LVEF) of <20% which returned back to normal LVEF of 57% after 10 days. Subsequent cardiac catheterisation showed non-obstructive coronaries. No specific therapy intended for reversal of SICM presents to date despite current sepsis survival guideline available for haemodynamic support. Initiation of beta blockers after recovery from septic shock has been beneficial.

17 A CASE OF TRANSIENT LEFT VENTRICULAR APICAL BALLOONING WITHOUT CORONARY ARTERY DISEASE

Introduction Several case series of transient left ventricular apical ballooning syndrome, also known as Tako-Tsubo cardiomyopathy, have been reported predominantly in the Japanese population. We present a white female patient with Tako-Tsubo cardiomyopathy in whom profoundly decreased glucose utilization was observed. Case Report A 52-year-old female with no previous cardiac history was brought to the emergency room twelve hours after the acute onset of chest pain and shortness of breath, which were triggered by an emotional argument with her husband. On arrival, her blood pressure was 77/50 mm Hg and heart rate was 88 beats/min. Jugular venous distention was appreciated in the sitting position and respiratory crackles were heard in bilateral lung fields. Electrocardiogram revealed mild ST elevation in leads II, III, aVF with diffuse T wave inversion. A chest radiograph was consistent with bilateral pulmonary parenchymal congestion. Emergent coronary angiography revealed normal coronary arteries. Left ventriculography showed distal anterior, apical and distal inferior akinesis with hyperkinesis of the remaining walls (Figures). Her serum troponin T was mildly elevated at 0.64 ng/mL. Over the next three days, she showed a marked clinical improvement with resolution of heart failure. Metabolic imaging with positron emission tomography (PET) revealed markedly reduced fluorine-18 fluorodeoxyglucose (FDG) uptake in the akinetic apical wall with relatively normal perfusion. Echocardiography was repeated three months later, which showed normalization of left ventricular wall motion. Repeat PET imaging revealed marked improvement of FDG uptake in the apical wall.