Biomedical subjects
Publications and source records attributed to Balendu C Vasavada.
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.
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.
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.
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.
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.
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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.
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.
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.
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.
OBJECTIVE: To study the effect of reinforcement as a quality improvement intervention in the evidence-based management of the coronary syndromes. METHODS: In the pre-intervention phase, the charts of 140 consecutive patients with ICD-9 codes 410-414 for coronary syndromes were reviewed for measurement of total cholesterol on admission and fasting low density lipoprotein (LDL) cholesterol, implementation of aspirin therapy on admission, beta-blockers' use during hospitalization, and treatment with angiotensin converting enzyme (ACE) inhibitors in patients with left ventricular systolic dysfunction. Reinforcement was used as an intervention for quality improvement. All personnel of Division of Cardiology including nursing staff, medical residents, cardiology fellows, and attending physicians were reinforced to adhere to the evidence-based management. In the post-intervention phase, charts of 140 consecutive patients with ICD-9 codes 410-414 for coronary syndromes were reviewed to assess the improvement in the same quality of care parameters. RESULTS: By reinforcement, a significant improvement was noted in all quality of care parameters studied. Proportion of patients who had total cholesterol measured on admission increased from 78% to 92% (P<0.005), and those who had fasting LDL cholesterol measured increased from 22% to 70% (P<0.0001). Use of aspirin at admission (in 74% of patients pre- vs. 80% of patients post-intervention, P<0.05), beta-blockers during hospitalization (in 62% of patients pre- vs. 78% of patients post-intervention, P<0.001), and ACE inhibitors in patients with left ventricular systolic dysfunction (in 58% of patients pre- vs. 89% of patients post-intervention, P<0.001) improved significantly after reinforcement to the medical personal. CONCLUSION: Reinforcement to adhere to the evidence-based management results in a significant improvement in the quality of care provided to the patients with coronary syndromes.
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.
Torsade de pointes is a form of polymorphic ventricular tachycardia occurring in a setting of prolonged QT interval on surface electrocardiogram. Congenital causes of prolonged QT interval occur in individuals with genetic mutations in genes that control expression of potassium and sodium channels and acquired causes are numerous, predominantly drugs causing prolonged QT interval by blockade of potassium channels. Among the drugs, antiarrhythmic agents most notably quinidine, sotalol, dofetilide and ibutilide have the potential to induce the fatal torsade de pointes. Many non-antiarrhythmic drugs can also cause torsade de pointes. Although it is important to distinguish between the congenital and the acquired forms of long QT syndrome as the later can often be reversed by correction of the underlying disorder or discontinuation of the offending drug, both forms are not mutually exclusive. Clinical considerations and management of torsade de pointes are described.
Echocardiography provides information regarding cardiac morphology, function and hemodynamics non-invasively. It is the most frequently performed cardiovascular examination after electrocardiography and chest X-ray. In less than half a century, this technique has evolved to a mainstay of cardiovascular medicine. The historical evolution of echocardiography is succinctly described including that of M-mode, two-dimensional, Doppler, stress, transesophageal, intraoperative, contrast, digital, three-dimensional and intracardiac echocardiography.
Large areas of non-functional but viable myocardium with reversible dysfunction are commonly seen in patients with acute myocardial infarction. Both reperfusion of acutely ischemic myocardium and chronic myocardial ischemia may produce a reversible forms of ventricular dysfunction. The two main conditions that lead to reversible myocardial dysfunction are stunned myocardium and hibernating myocardium. Myocardial stunning represents post-ischemic myocardial dysfunction that persists despite restoration of normal flow, with gradual return of contractile function. Hibernating myocardium is a state of persistently impaired myocardial function at rest due to reduced coronary blood flow owing to residual stenosis that can be restored toward normal by revascularization. The success of the revascularization procedures depends on the presence of amount of dysfunctional but viable myocardium. The basics and evaluation of reversible myocardial dysfunction are reviewed.
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Intracoronary brachytherapy has emerged as one of the novel exciting developments in the field of interventional cardiology to counteract the problem of restenosis. Restenosis is the major limitation to a full expansion of all revascularization procedures. Elastic recoil, unfavorable remodeling and a proliferative response to injury are the more importune mechanisms to restenosis. The technique of intracoronary brachytherapy involves application of locally delivered radiation or brachytherapy in the management of restenosis. Ionizing radiation has been shown to decrease the proliferative response to injury in animal models of restenosis. Subsequently, several small randomized trials have demonstrated that intracoronary brachytherapy can reduce the rates of both angiographic and clinical restenosis in patients undergoing percutaneous coronary intervention for in-stent restenosis.
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