Role of electrocardiography in identifying right ventricular dysfunction in acute pulmonary embolism.

The role of electrocardiography in identifying right ventricular (RV) dysfunction in acute pulmonary embolism (APE) was evaluated in 81 patients with APE. The electrocardiographic markers studied were T-wave inversion in leads V1 to V3, the S1Q3T3 pattern, right bundle branch block, and sinus tachycardia. T-wave inversion in leads V1 to V3 had the greatest sensitivity and diagnostic accuracy for identifying RV dysfunction in patients with APE. The S1Q3T3 pattern and right bundle branch block had good specificity but moderate accuracy.

Treatment of refractory angina pectoris.

Refractory angina pectoris is defined as Canadian Cardiovascular Society class III or IV angina, where there is marked limitation of ordinary physical activity or inability to perform ordinary physical activity without discomfort, with an objective evidence of myocardial ischemia and persistence of symptoms despite optimal medical therapy, life style modification treatments, and revascularization therapies. The patients with refractory angina pectoris may have diffuse coronary artery disease, multiple distal coronary stenoses, and or small coronary arteries. In addition, a substantial portion of these patients cannot achieve complete revascularization and continue to experience residual anginal symptoms that may impair quality of their life and increase morbidity. This represents an end-stage coronary artery disease characterized by a severe myocardial insufficiency usually with impaired left ventricular function. As the life expectancy is increasing, patients with angina pectoris refractory to conventional antianginal therapeutics are a challenging problem. We review the nonconventional therapies to treat the refractory angina pectoris, including pharmacotherapy, therapeutic angiogenesis, transcutaneus electrical nerve and spinal cord stimulation, enhanced external counterpulsation, surgical transmyocardial laser revascularization, percutaneous transmyocardial laser revascularization, percutaneous in situ coronary venous arterializations, and percutaneous in situ coronary artery bypass. These therapies are not supported by a large body of data and have only a complementary role; therefore, the aggressive traditional and proven treatment of angina pectoris should be continued along with these therapies, used on an individual basis.

Cardiac troponin I release in acute pulmonary embolism in relation to the duration of symptoms.

PURPOSE: To evaluate the release of cardiac troponin I in normotensive patients with acute pulmonary embolism in relation to the duration of symptoms. METHODS: Fifty-seven normotensive patients with acute pulmonary embolism were included in the study. Patients were divided into two groups based on the duration of symptoms at presentation: symptoms of < or =72 h, group A; symptoms of >72 h, group B. Serum cardiac troponin I levels were measured at presentation. RESULTS: Mean age was 63+/-18 years and 23 (40%) patients were males. Thirty-three (58%) patients had symptoms of < or =72 h (group A) and 24 (42%) had symptoms of >72 h (group B). Both groups had similar prevalence of right ventricular dysfunction on echocardiography (55% [n=18] in group A vs. 42% [n=10] in group B, p=NS). Sixteen patients had elevated serum cardiac troponin I (mean+/-S.D. 3.3+/-2.3 ng/ml, range 0.6-8.3 ng/ml). Elevated serum cardiac troponin I was strongly associated with right ventricular dysfunction (p=0.015). All patients with elevated serum cardiac troponin I (n=16) were in group A (p<0.0001). Twelve of 18 (67%) patients with (p=0.0005) and 4 of 15 (27%) patients without (p=NS) right ventricular dysfunction had elevated serum cardiac troponin I. Thirteen of 16 (81%) patients with elevated serum cardiac troponin I had duration of symptoms < or =24 h at presentation. CONCLUSIONS: The dynamics of cardiac troponin I release in acute pulmonary embolism in patients who present with symptoms of < or =72 h duration could be different from those who present with longer duration of symptoms. Therefore, the use of cardiac troponin I in risk stratification of acute pulmonary embolism might be limited to the patients presenting within 72 h of the onset of symptoms.

Acute pulmonary embolism in elderly: clinical characteristics and outcome.

OBJECTIVE: To evaluate the clinical characteristics and outcome of acute pulmonary embolism in elderly in comparison to the younger patients. METHODS: Study population consisted of 136 patients with a confirmed diagnosis of acute pulmonary embolism. Clinical characteristics and thromboembolic risk factors were analyzed between the elderly (> or =65 years of age) and the younger (<65 years of age) patients. In-hospital mortality was used as a measure of outcome. RESULTS: Elderly group consisted of 70 patients (age 76.4+/-8.3 years, range 65-96 years; females 58%) and younger group of 66 patients (age 48.5+/-12 years, range 18-64 years, females 59%). Syncope was more frequent in elderly group (19% vs. 6%, P=0.03) but the symptoms of shortness of breath and pleuritic chest pain were not significantly different between groups. Malignancy was the most common risk factor for thrombo-embolism, but immobilization predominated among patients in elderly group (21% vs. 6%, P=0.01). Tachycardia was common in younger patients compared to the elderly. Ventilation-perfusion scan was used more commonly in younger patients (76% vs. 57%, P=0.02), whereas, helical computed-tomography scan was used equally in both groups. Most of the patients had lower extremity duplex study (97% in each group). Inferior vena cava filter placement was common and thrombolytic therapy rare among elderly patients. Patients in elderly group had higher in-hospital mortality (17% vs. 5%, P=0.02). CONCLUSIONS: Syncope is a more frequent presenting symptom and immobilization a common risk factor in elderly patients with acute pulmonary embolism. In addition, they have higher in-hospital mortality.

Early twentieth century descriptions of the Chagas heart disease.

Chagas heart disease is endemic in 21 countries with approximately 100 million people at risk. It is the most common cause of myocarditis in the Americas and is recognized to have existed for more than 4000 years (isolated from mummies). Chagas disease was discovered during the search to find a cause for the overwhelming deaths occurring in Brazil in the late 18th century. Physician Carlos Chagas discovered Trypanosome minasense in 1908 while researching on malaria. Subsequently, the existence of the barbeiro triatomine (insects bites on the face), the isolation of the Trypanosome cruzi in the triatomine and the first human description of a disease in a 9-month-old child depicted the existence of a new human trypanosomiasis. Chagas named the trypanosome species after his colleague and mentor Oswaldo Cruz. In subsequent papers, Chagas described the morphology and evolutionary cycle of the trypanosome and the clinical features of the disease, including involvement of the heart. Never before or since one physician has fully characterized a disease from its grass roots to the clinical forms more or less all by himself.

Female preponderance in ibutilide-induced torsade de pointes.

OBJECTIVE: Ibutilide, a class III antiarrhythmic agent used for pharmacological cardioversion of atrial arrhythmias, has a potential to cause QT-interval prolongation and torsade de pointes. Purpose of this study was to determine whether women are more prone to develop ibutilide-induced torsade de pointes. METHODS: All clinical trials, cases, case series, and related articles in English-language in addition to 51 patients from our institution on the subject were examined. RESULTS: In a database derived from 23 reports in literature and from our institution, 1720 patients received ibutilide for cardioversion of atrial arrhythmias. Only in 87% (n=1492) patients, data were reported whether or not ibutilide caused torsade de pointes. The overall incidence of torsade de pointes was 3.9% (n=58) patients. Data on sex distribution of ibutilide-induced torsade de pointes was available in 73% (n=1096) patients. Torsade de pointes developed in 17 (5.6%) of 304 women and 24 (3%) of 792 men (P=0.05). It occurred during or within 45 min after completion of the infusion of ibutilide. Treatment instituted was with intravenous magnesium sulfate alone in 14% (n=8) patients, magnesium sulfate plus lidocaine in 5% (n=3) patients, magnesium sulfate with electrical cardioversion in 17% (n=10) patients, electrical cardioversion alone in 19% (n=11) patients, and precordial thump in 3% (n=2) patients. In 41% (n=24) of patients who developed torsade de pointes, it resolved without treatment. There were no reported deaths secondary to torsade de pointes associated with ibutilide infusion. CONCLUSION: Incidence of ibutilide-induced torsade de pointes is higher in women than in men. Greater caution must be observed while using ibutilide in women.

Elevated serum cardiac troponin I in rhabdomyolysis.

OBJECTIVE: To examine the etiology and clinical significance of elevated serum cardiac troponin I (cTnI) in patients with rhabdomyolysis. METHODS: Data on 91 (63 men) consecutive patients with rhabdomyolysis were examined. RESULTS: The mean age was 57.8+/-19.6 years (range 24-97 years). Patients were divided into two groups: cTnI-positive with serum cTnI >0.6 ng/ml (n=19) and cTnI-negative with serum cTnI <0.6 ng/ml (n=72). Prevalence of cardiovascular risk factors was equal in both groups. Illicit substance use was more common in the cTnI-positive group (31% vs. 14%, P=0.04). Peak creatine kinase (CK) was higher in cTnI-positive group (34,811+/-38,309 vs. 15,070+/-21,655 U/l, P=0.04) but there was no difference in the MB isoenzyme (CK-MB) (118+/-132 vs. 89+/-451 ng/ml, P=0.63). In cTnI-positive group, there was a strong correlation between peak CK and CK-MB (r(2)=0.606, P=0.00008) but not between peak cTnI and peak CK (r(2)=0.164 and P=0.08) or CK-MB (r(2)=0.134 and P=0.12) levels. Serum creatinine was higher in cTnI-positive group (3.58+/-2.73 vs. 1.83+/-2.01 mg/dl, P=0.02) but there was no correlation between serum creatinine and cTnI (r(2)=0.121, P=0.158). None of the cTnI-positive patient had segmental wall motion abnormalities. Seventeen (89%) patients in cTnI-positive and 19 (26%) in cTnI-negative group required admission to intensive care unit (P=0.0001). Hypotension (37% vs. 6%, P=0.0002) and sepsis (47% vs. 11%, P=0.0003) were more common in cTnI-positive group. Duration of hospitalization was longer in cTnI-positive group (17.7+/-11.7 vs. 8.9+/-13 days, P=0.007) but there was no significant difference in mortality. CONCLUSION: In rhabdomyolysis, serum cTnI may be elevated unrelated to the degree of muscle damage, renal failure and cardiovascular risk factors, and is likely related to the etiology of rhabdomyolysis, as is evidenced by significantly higher serum cTnI with illicit substance use, hypotension, and sepsis. Elevated serum cTnI is associated with a higher morbidity.

Positional ventricular tachycardia from a fractured mediport catheter with right ventricular migration--a case report.

The totally implantable catheter system has gained popularity as venous access when prolonged treatment is needed. Despite its frequent use, intravascular fracture and embolization of catheter fragments from implantable venous port-catheter systems present a rare but potentially life-threatening complication. Any implanted catheters should therefore be removed after completion of the treatment or the system's integrity should be monitored on a regular basis. This report illustrates such a case, which presented with ventricular tachycardia triggered by changes in body position from a fractured Mediport catheter with cardiac migration. A 34-year-old woman had a venous port catheter (Mediport) implanted into the right subclavian vein for neoadjuvant radio-chemotherapy for Hodgkin's lymphoma. Owing to the patient's difficult venous access the catheter was left in situ after treatment. Three years after insertion of the Mediport she presented with shortness of breath and palpitations when lying in the left lateral position. Physical examination revealed no abnormalities. An electrocardiogram was within normal rhythm. An outpatient Holter monitor revealed multiple episodes of nonsustained and sustained ventricular tachycardia triggered by lying in the left lateral position. A chest radiograph showed a normal location of the port-system, but the distal fragment of the catheter had embolized into the right ventricle. The embolized fragment was extracted with a gooseneck snare technique and the reservoir of the system was removed under local anesthesia without any complications. The patient was free of symptoms at 7 seven months follow-up.

Clinical aspects of the Chagas' heart disease.

Chagas' heart disease, caused by protozoan Trypanosoma cruzi, is a common cause of cardiomyopathy in the Americas. Transmission of T. cruzi occurs through Reduviids, the kissing bugs. Less common ways of transmission are blood transfusion, congenital transmission, organ transplantation, laboratory accident, breastfeeding, and oral contamination. Infestation results in cardiac dysautonomia, myocardial apoptosis, and myocardial fibrosis. In acute phase, death is mostly caused by myocarditis and in chronic phase, it is mostly by irreversible cardiomyopathy. A majority of the patients with Chagas' disease remain in the latent phase of disease for 10 to 30 years or even for life. Specific anti-Chagas' therapy with trypanocide drugs is useful in acute phase but the management of chronic Chagas' heart disease is mostly empirical. The mortality during the acute phase of cardiac Chagas is around 5%. Five-year mortality of chronic Chagas' disease with cardiac dysfunction is above 50%. The clinical aspects of the Chagas' heart disease are concisely reviewed.

Delayed presentation of calcium channel antagonist overdose.

The calcium channel antagonists are generally safe in therapeutic dosage, but severe side effects with elevated intake are increasingly described. Typical features include confusion, lethargy, hypotension, sinus node depression, and cardiac conduction defects. Even if patients are stable on presentation, this does not preclude the possible late development of adverse events from the long-acting formulations of calcium channel blockers. A case of toxic overdose with 1440 mg of slow-release diltiazem is presented; this patient was stable on presentation, but rapidly became hemodynamically unstable, requiring treatment with intravenous calcium, temporary pacemaker, inotropic support and mechanical ventilation with a successful outcome. A concise review of the therapeutic considerations is provided.

QT interval prolongation with global T-wave inversion: a novel ECG finding in acute pulmonary embolism.

OBJECTIVE: The purpose of this study was to report a novel electrocardiographic (ECG) phenomenon in acute pulmonary embolism characterized by QT interval prolongation with global T-wave inversion. METHODS: Among a total of 140 study patients with a confirmed diagnosis of acute pulmonary embolism, patients who fulfilled the inclusion criteria for QT interval prolongation with global T-wave inversion were examined. Each of these patients had undergone a detailed clinical evaluation including testing for myocardial injury and echocardiography. RESULTS: QT interval prolongation with global T-wave inversion was found in five patients (age 51-68 years) with acute pulmonary embolism. Four were women. Acute pulmonary embolism was diagnosed by ventilation-perfusion scan in three patients and by spiral computed tomography in other two patients. None of the patients had any right or left ventricular regional wall motion abnormalities on echocardiography. All patients had changes characteristic of hemodynamically significant pulmonary embolism, including right ventricular stunning or hypokinesis and dilatation in five patients with paradoxical septal motion in four. Acute coronary syndrome was ruled out in each patient by clinical evaluation, serial ECGs and cardiac markers, and lack of regional wall motion abnormalities on echocardiography. Prolongation of QT intervals (QTc 456-521 ms) with global T-wave inversion was noted on presentation. The ECG changes gradually resolved in 1 week in all patients with appropriate treatment of acute pulmonary embolism. One patient died. None of the patients developed torsade de pointes. CONCLUSIONS: Acute pulmonary embolism may occasionally result in reversible QT interval prolongation with deep T-wave inversion, and, thus should be considered among the acquired causes of the long QT syndrome.

Ibutilide for pharmacological cardioversion of atrial fibrillation and flutter: impact of race on efficacy and safety.

OBJECTIVE: To evaluate the racial differences in the efficacy and safety of ibutilide in patients with recent-onset (<2 weeks) atrial fibrillation and atrial flutter. METHODS: This study included 58 consecutive patients with recent-onset atrial fibrillation (n = 34) and atrial flutter (n = 24). The mean age was 65.7 +/- 14.6 years (range, 37-86 years), 47% were women (n = 27) and 34% (n = 20) were African Americans. The duration of arrhythmia ranged from 3 hours to 2 weeks. All patients had echocardiography, were on therapeutic anticoagulation, had a fairly well controlled ventricular rate, normal QTc interval on 12-lead electrocardiography, and normal serum electrolytes. Ibutilide was administered as an intravenous infusion with a maximal dose of 2 mg. RESULTS: The overall conversion rate to sinus rhythm was 66% (n = 38), with 62% (n = 21) with atrial fibrillation and 71% (n = 17) of atrial flutter. Most conversions (84%) occurred within 45 minutes of ibutilide infusion. The mean time to arrhythmia conversion was 37.4 +/- 59.8 minutes. Race had a significant impact on efficacy, with increased conversions seen in African Americans (P = 0.004) and increased nonconversion seen in whites (P = 0.02). Successful conversion was not affected by the left atrial size or the presence of valvular heart disease, hypertension, heart failure, coronary heart disease, and diabetes mellitus. QTc intervals were prolonged after drug administration, with a mean change of 24.6 milliseconds for all patients. The QTc prolongation after drug administration was greater in African Americans than in whites (27.4 vs. 23.3 milliseconds). Torsade de pointes occurred in 4 patients (3 African Americans) and was treated with intravenous magnesium sulfate and electrical cardioversion. CONCLUSION: Ibutilide used for pharmacological cardioversion of atrial fibrillation and atrial flutter is more effective in African Americans but carries a higher risk of torsade de pointes.

Use of ibutilide for cardioversion of recent-onset atrial fibrillation and flutter in elderly.

Ibutilide is a class III antiarrhythmic drug used for pharmacological cardioversion of recent-onset atrial fibrillation and flutter. The objective of the study was to assess the efficacy of ibutilide in elderly patients (age, >or=65 years). The study population consisted of 32 consecutive elderly patients (17 women, 15 men; mean age, 76 +/- 8 years; age range, 65-94 years) with recent-onset atrial fibrillation (19 patients) or flutter (13 patients). Ibutilide was administered 1-mg intravenously over 10 minutes, and a second 10-minute infusion of 1-mg was given if the arrhythmia did not terminate within 10 minutes after the end of initial infusion. Twenty-six patients received two 1-mg doses of ibutilide. The rate of successful arrhythmia termination was 59% (19 patients): 63% in patients with atrial fibrillation (12 of 19) and 54% in atrial flutter (7 of 12). The mean conversion time was 33 +/- 45 minutes. Three-fourths of the conversions occurred within 45 minutes of treatment. No clinical variables were correlated with success of cardioversion. Patients with a left atrial size of 50 mm or larger had a conversion rate of 50% compared with a conversion rate of 61% in patients with a left atrial size of less than 50 mm (P = NS). Ibutilide-induced lengthening in the QTc interval was of 17 +/- 21 milliseconds. Cardiac complications were torsade de pointes (1 patient), nonsustained ventricular tachycardia (1 patient), and transient bradycardia (1 patient). Torsade de pointes was terminated with direct current cardioversion. Ibutilide appears to be an effective drug for conversion of recent-onset atrial fibrillation and flutter in elderly patients under monitored conditions. Complications are rare and transient.

Ibutilide-induced long QT syndrome and torsade de pointes.

Ibutilide is a class III antiarrhythmic agent used for the termination of atrial fibrillation and atrial flutter. It mainly affects membrane potassium currents and prolongs the cardiac action potential. This effect is reflected as QT interval prolongation on the surface electrocardiogram. Like other drugs that affect potassium currents, ibutilide is prone to induce a malignant ventricular tachycardia, torsade de pointes. We report four cases of torsade de pointes after administration of ibutilide for pharmacologic cardioversion of atrial fibrillation and atrial flutter; three of these cases required direct current cardioversion for termination of torsade de pointes. All four patients were female. We discuss the risk factors for development of ibutilide-induced torsade de pointes.