CT angiography images of an anomalous right coronary artery.

We describe a 33-year-old male with angina pectoris who was found to have abnormal origin and course of right coronary artery from left aortic cusp. The abnormal origin was identified by conventional coronary angiography but the abnormal course of the vessel between ascending aorta and the main pulmonary artery was precisely delineated by high resolution CT angiography. Patient underwent successful surgical transposition of the anomalous vessel with complete resolution of symptoms.

Cardiac troponin I in sickle cell crisis.

Gross and microscopic findings consistent with acute and healed myocardial injury without coronary artery disease have been described in autopsy studies of patients with sickle cell crisis. The present study was designed to determine whether serum levels of cardiac troponin I are elevated in sickle cell crisis. Cardiac troponin I levels were measured in 32 patients age>18 years with the admission diagnosis of sickle cell crisis. All patients had cardiac troponin I level drawn >24 h after the onset of symptoms. The clinical profile and electrocardiograms were analyzed. Out of 32 patients, 2 patients had serum cardiac troponin I elevated, both had presented with acute chest syndrome. Serum cardiac troponin I may be elevated during sickle cell crisis, possibly by myocardial ischemia resulting from microvascular coronary obstruction during sickle cell crisis.

Cardiovocal syndrome: a systematic review.

Hoarseness associated with mitral stenosis was initially described by Ortner. Several cardiopulmonary conditions were associated with left recurrent laryngeal nerve palsy over the last 100 years; thus, the syndrome is termed as cardiovocal syndrome or Ortner's syndrome. This study aimed to classify the various predisposing conditions and to explain the pathophysiology and treatment opportunities available for these patients.

Prosthetic heart valves: types and echocardiographic evaluation.

In the last five decades multiple different models of prosthetic valves have been developed. The purpose of this article is to provide a comprehensive source of information for the types and the echocardiographic evaluation of the prosthetic heart valves.

Unique wall motion abnormalities on stress echocardiogram associated with Wolff-Parkinson-White pattern electrocardiogram: a case report.

Preexcitation syndromes pose a diagnostic challenge for exercise stress testing. We present stress echocardiographic findings in patient with Wolff-Parkinson-White (WPW) pattern on surface electrocardiogram (EKG). Echocardiogram at rest demonstrated paradoxical septal motion which disappeared during peak exercise and reappeared during rest. Preexcitation pattern on EKG also disappeared at peak stress. We tried to explain the underlying mechanisms of the above abnormality and the usefulness of stress testing in this group of patients.

Benazepril induced isolated visceral angioedema: a rare and under diagnosed adverse effect of angiotensin converting enzyme inhibitors.

Angiotensin converting enzyme inhibitors are one of the most commonly prescribed medications and angioedema of upper aerogastric tracts is a well recognized complication. Isolated visceral angioedema with the use of angiotensin converting enzyme inhibitors is rare and is relatively under diagnosed. The visceral angioedema should be considered in patients taking angiotensin converting enzyme inhibitors who develop gastrointestinal complaints. We report a case of subacute intestinal obstruction from the use of benazepril, which was promptly resolved after withdrawing benazepril.

Candida parapsilosis endocarditis 8 months after transient candidemia.

We report a case of aortic valve endocarditis with aortic root abscess from Candida parapsilosis occurring 8 months after transient candidemia. Despite the fact that the patient was treated appropriately, candidemia persisted and later on presented with an embolic stroke as a complication of fungal endocarditis.

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.

Cardiac troponin I release in non-ischemic reversible myocardial injury from parvovirus B19 myocarditis.

Cardiac troponin I is released from myocytes in both reversible and irreversible myocardial injury. The changes in myocyte membrane permeability resulting from the injury could be enough for the release of cardiac troponins from the free cytosolic pool of myocytes without structural damage. We report a case of parvovirus B19 myocarditis in a 26-year-old male who developed regional wall motion abnormalities and severe left ventricular systolic dysfunction with elevated serum levels of cardiac troponin I (peak=11.7 ng/ml). Diagnosis of parvovirus myocarditis was confirmed by presence of high titers of parvovirus B19 IgG and identification of parvovirus B19 DNA by polymerase chain reaction. Within a few days of supportive treatment, the regional wall motion abnormalities resolved, the cardiac function recovered, and the elevation in serum cardiac troponin I subsided. This case further denotes the possibility of release of cardiac troponin I in non-ischemic, reversible myocardial injury.

Hypothermia: evaluation, electrocardiographic manifestations, and management.

Hypothermia-related cases typically occur after exposure to low ambient temperatures; however, numerous cases occur in individuals with no history of exposure to cold environment. Hypothermia is associated with such complications as acidosis, impaired myocardial function, bleeding diathesis, and decreased kidney and liver function. The well-known electrocardiographic manifestations of hypothermia are the presence of J (Osborn) waves, prolonged PR, QRS, and QT intervals, and atrial arrhythmias. The choice of rewarming therapy is based on the degree of hypothermia. The evaluation, electrocardiographic manifestations, and management of hypothermia are reviewed.

Cardiac effects of acute myelitis.

Neurogenic stunned myocardium has been described in association with subarachnoid hemorrhage, Guillain-Barre syndrome, and metastatic brain tumors. We describe a case of neurogenic stunned myocardium associated with acute myelitis. A 27-year-old female presented with acute onset of quadriplegia, sensory deficit, and acute pulmonary edema. Magnetic resonance imaging was consistent with acute myelitis. Echocardiogram showed left ventricular ejection fraction of 35% with moderate to severe global hypokinesis. During the course of admission, she had several episodes of sinus bradycardia and high degree atrioventricular block. All cardiac abnormalities resolved completely in eight days of admission.

Coronary artery fistulas: clinical and therapeutic considerations.

Coronary artery fistulas vary widely in their morphological appearance and presentation. These fistulas are congenital or acquired coronary artery abnormalities in which blood is shunted into a cardiac chamber, great vessel, or other structure, bypassing the myocardial capillary network. The majority of these fistulas arise from the right coronary artery and the left anterior descending coronary artery; the circumflex coronary artery is rarely involved. Clinical manifestations vary considerably and the long-term outcome is not fully known. The patients with coronary fistulas may present with dyspnea, congestive heart failure, angina, endocarditis, arrhythmias, or myocardial infarction. A continuous murmur is often present and is highly suggestive of a coronary artery fistula. Differential diagnosis includes persistent ductus arteriosus, pulmonary arteriovenous fistula, ruptured sinus of Valsalva aneurysm, aortopulmonary window, prolapse of the right aortic cusp with a supracristal ventricular septal defect, internal mammary artery to pulmonary artery fistula, and systemic arteriovenous fistula. Although noninvasive imaging may facilitate the diagnosis and identification of the origin and insertion of coronary artery fistulas, cardiac catheterization and coronary angiography is necessary for the precise delineation of coronary anatomy, for assessment of hemodynamics, and to show the presence of concomitant atherosclerosis and other structural anomalies. Treatment is advocated for symptomatic patients and for those asymptomatic patients who are at risk for future complications. Possible therapeutic options include surgical correction and transcatheter embolization. Historical perspectives, demographics, clinical presentations, diagnostic evaluation, and management of coronary artery fistula are elaborated.

Hyperkalemia induced failure of atrial and ventricular pacemaker capture.

Hyperkalemia is a life threatening metabolic condition. The common risk factors for hyperkalemia include renal insufficiency, use of angiotensin converting enzyme inhibitors, potassium supplementation and excessive consumption of potassium containing diet. A mild to moderate increase in serum potassium causes an increase in myocardial excitability, but further increase leads to impaired myocardial responsiveness, including that to pacing stimulation. Hyperkalemia has been reported to cause failure of atrial capture due to pacemaker exit block. We report a case where hyperkalemia resulted in failure of both the atrial and the ventricular pacemaker capture.

Staphylococcus aureus infective endocarditis and septic pulmonary embolism after septic abortion.

We report a case of a 26-year-old female who after septic abortion developed tricuspid valve endocarditis with large vegetations, which subsequently resulted in embolism to right main pulmonary artery. Patient was treated with intravenous antibiotics and had a good recovery.

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.

QT interval prolongation in diphenhydramine toxicity.

Diphenhydramine overdose in one of the frequent reported causes of acute poisoning. Patients with diphenhydramine overdose can present with central nervous system manifestations, anticholinergic manifestations and cardiovascular symptoms. The cardiovascular symptoms of diphenhydramine overdose include myocardial depression and refractory hypotension. Massive ingestions have been reported to cause myocardial depressant effect with widening of QRS complex and prolonged QT interval on electrocardiogram. We report an adolescent male with moderate diphenhydramine ingestion, who was found unresponsive with seizure like activity. Electrocardiogram on presentation showed wide complex tachycardia with right bundle branch block pattern and QT interval prolongation. These changes reverted to normal with treatment. Diphenhydramine overdose may occasionally result in prolongation of QT interval.