PubMed Health⌕ Search

Biomedical subjects

Ramesh M Gowda

Publications and source records attributed to Ramesh M Gowda.

At least 37 records · Page 2Linked to original sources

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.

Anti-Arrhythmia Agents↗

Reinforcement as a means for quality improvement in management of coronary syndromes: adherence to evidence-based medicine.

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.

Adult↗

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.

Cardiology↗

Takayasu arteritis of subclavian artery in a Caucasian.

Takayasu arteritis, an inflammatory and obliterative disease of medium and large arteries, is classified as a giant cell arteritis. It has a predilection for the aortic arch, its main branches, and coronary and pulmonary arteries. The early symptoms of Takayasu arteritis may be mainly systemic and may resemble polymyalgia rheumatica. The etiology is unknown but autoimmunity has been suggested to play a role. Diagnosis is based on symptoms, physical findings, and imaging, because tissue diagnosis is rarely feasible. Unlike atherosclerotic vascular disease, Takayasu arteritis affects primarily, but not exclusively, young women. Contrary to earlier reports, it is not limited to the women of Japanese origin but is present worldwide. The current report is of a Caucasian woman who presented with nonspecific complaints of upper back pain, weakness, malaise, and fatigue. Her physical examination revealed absent left radial pulse and a blood pressure differential, later confirmed by radiological imaging studies to be due to left subclavian artery stenosis consistent with Takayasu arteritis. The presentation and management of the patient is described, and Takayasu arteritis is succinctly reviewed.

Adult↗

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.

Adult↗

Torsade de pointes: the clinical considerations.

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.

Electrocardiography↗

Magnesium in treatment of acute myocardial infarction.

Magnesium has properties of myocardial cytoprotection, the pathophysiological explanations of which in acute myocardial infarction include prevention of arrhythmia, antiplatelet effect, prevention of reperfusion injury, and coronary vasodilation. Although several studies have evaluated the role of magnesium administration in patients with acute myocardium infarction, the clinical impact of such a therapy in this condition has been controversial, largely as a result of conflicting data from randomized controlled trials. The data available to date do not favor the routine administration of intravenous magnesium in patients with myocardial infarction, but this should not preclude magnesium administration to replenish low serum magnesium concentrations or use of magnesium sulfate for treatment of torsade de pointes in patients with myocardial infarction.

Humans↗

History of the evolution of echocardiography.

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.

Echocardiography↗

Acute ventricular rate control in atrial fibrillation and atrial flutter.

Atrioventricular node blocking agents including beta-adrenergic blockers, non-dihydropyridine calcium channel blockers and digoxin are usually effective in controlling ventricular rate in atrial fibrillation and flutter. Intravenous beta-blockers and non-dihydropyridine calcium channel blockers are equally effective in rapidly controlling the ventricular rate. The addition of digoxin to the regimen causes a favorable outcome but digoxin as a single agent is generally less effective in slowing the ventricular rate in acute setting. Clonidine, magnesium, and amiodarone have also been used for acute ventricular rate control in atrial fibrillation. Limited data suggest that combination regimens provide better ventricular rate control than any agent alone. The agent of first choice is usually individualized depending upon the clinical situation. Beta-blockers are preferable in patients with myocardial ischemia, myocardial infarction and hyperthyroidism and in post-operative state, but should be avoided in patients with bronchial asthma and chronic obstructive pulmonary disease where non-dihydropyridine calcium channel blockers are preferred. Beta-blockers are preferred drugs used for acute ventricular rate control in atrial fibrillation during pregnancy. In atrial fibrillation with Wolff-Parkinson-White syndrome, beta-blockers, calcium channel blockers and digoxin should be avoided, as these drugs are selective atrioventricular node blockers without slowing conduction through the accessory pathway, which can lead to increased transmission of impulses preferentially through the accessory pathway and precipitate ventricular fibrillation. The drug of choice for atrial fibrillation in pre-excitation syndrome is procainamide but propafenone, flecainide and disopyramide have also been used. When clinical condition is unstable or patient is hemodynamically compromised, immediate electrical cardioversion is the treatment of choice, as the best measure to control ventricular rate is by conversion to sinus rhythm. Factors precipitating rapid ventricular rate should be treated as well.

Atrial Fibrillation↗

Reversible myocardial dysfunction: basics and evaluation.

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.

Coronary Circulation↗

Calcifications of the heart.

Cardiac calcification usually represents the result of a pathologic process. Some forms of calcification represent chronic change in an ageing population, and must be differentiated from pathologic calcification. Still other forms of calcification are associated with ageing and chronic degeneration, but also reflect ongoing pathologic processes. Recognition of cardiac calcification may be an early sign or only sign of a pathologic process. Characterization of the calcification in terms of its distribution and appearance is a helpful means for determining which structures are calcified, differentiating pathologic from nonpathologic processes. This article provides an overview of the types of calcifications of the heart, pathogenesis, and utility of the various imaging modalities for their detection.

Calcinosis↗

Efficacy and safety of endovascular intracoronary brachytherapy.

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.

Brachytherapy↗

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.

Acute Disease↗

Left bundle branch block in type 2 diabetes mellitus: a sign of advanced cardiovascular involvement.

OBJECTIVE: To evaluate left bundle branch block (LBBB) as an indicator of advanced cardiovascular involvement in diabetic (DM) patients by examining left ventricular systolic function and proteinurea. METHODS: Data of 26 diabetic patients with left bundle branch block (DM with LBBB) were compared with data of 31 diabetic patients without left bundle branch block (DM without LBBB) and 18 nondiabetic patients with left bundle branch block (non-DM with LBBB). The inclusion criteria were age >45 years, and diabetes mellitus type 2 of >5 years. RESULTS: Mean ages of patients in DM with LBBB, DM without LBBB, and non-DM with LBBB groups were 67 +/- 8, 68 +/- 10, and 65 +/- 10 years, respectively (P = NS). Females were 65%, 61%, and 61%, respectively (P = NS). Left ventricular ejection fraction in DM with LBBB was significantly lower than in DM without LBBB and non-DM with LBBB (30 +/- 10% vs 49 +/- 12% and 47 +/- 8%, P < 0.01). Left ventricular end-diastolic volume was significantly higher in DM with LBBB than in DM without LBBB and non-DM with LBBB (188.6 +/- 16.4 mL vs 147.5 +/- 22.3 mL and 165.3 +/- 15.2 mL, P < 0.03). Similarly, left ventricular end-systolic volume was significantly higher in DM with LBBB than in DM without LBBB and non-DM with LBBB (135.4 +/- 14.7 mL vs 83.7 +/- 9.5 mL and 96.6 +/- 18.4 mL, P < 0.02). No statistically significant difference was seen in left atrial size. Proteinurea in DM with LBBB (79.4 +/- 18.9 mg/dL) was significantly higher than in DM without LBBB (35.6 +/- 8.5 mg/dL, P < 0.05) and non-DM with LBBB (12 +/- 3.5 mg/dL, P < 0.05); however, there was no significant difference in Hb A1c levels in DM with LBBB and DM without LBBB (9.01% vs 7.81%, P = NS). CONCLUSIONS: Left bundle branch block in diabetic patients indicates advanced cardiovascular involvement manifesting with more severe left ventricular systolic dysfunction and proteinurea compared to both diabetic patients without left bundle branch block and nondiabetic patients with left bundle branch block.

Aged↗

Survival of an octogenarian after rupture of the left ventricular free wall caused by myocardial infarction.

Left ventricular free wall rupture is an uncommon complication after a myocardial infarction that is associated with a high mortality rate from pericardial tamponade, especially in the elderly. Early recognition and management of this clinical entity affects the outcome; therefore, a high index of suspicion is imperative. We present a case of an 80-year-old man admitted with myocardial infarction, who had subsequent findings of left ventricular free wall rupture complicated by pericardial tamponade. Emergent surgical repair led to successful recovery. A brief overview of the clinical presentation, diagnosis, and management of this challenging and potentially fatal complication is presented.

Age Factors↗