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K Shivkumar

Publications and source records attributed to K Shivkumar.

17 recordsLinked to original sources
PubMed2001

Apoptosis in the genesis of cardiac rhythm disorders.

Programmed cell death has provided a potential pathogenetic mechanism that could play a role in several diseases of the cardiac conduction system and the myocardium that are clinically expressed as disorders of the cardiac rhythm (Fig. 4). Most of these studies have been descriptive. The exact nature of the triggers for apoptotic cell death is not well understood and is a subject of current investigation. Alterations in the architecture of the myocardium play an important role in the pathogenesis of ventricular arrhythmias that are responsible for a large proportion of sudden cardiac deaths. Although apoptosis is essential for normal development, excessive apoptosis resulting from pathological triggers may result in destruction of tissues and in the development of heart disease in which a fatal arrhythmic event may be a final common pathway. At present, the triggers for programmed cell death in disorders of the cardiac rhythm are not understood completely. Because diverse conditions trigger apoptosis, treatment strategies may have to be directed toward attenuating such triggers and, in some instances, toward modifying the process itself. If future therapies that can favorably modulate the apoptotic process in conditions such as dilated cardiomyopathy and postmyocardial infarction are developed, they will have the potential to prevent the pathologic alteration of myocardial architecture that is conducive to arrhythmogenesis.

Apoptosis↗
PubMed2001

Initial experience with an active-fixation defibrillation electrode and the presence of nonphysiological sensing.

Nonphysiological sensing by a pacing and defibrillation electrode may result in inappropriate defibrillator discharges and/or inhibition of pacing. Active-fixation electrodes may be more likely to sense diaphragmatic myopotentials because of the protrusion of the screw for fixation. In addition, the movement of the fixation screw in an integrated bipolar lead system could also result in inappropriate sensing. This may be increasingly important in patients who are pacemaker dependent because the dynamic range of the autogain feature of these devices is much more narrow. Five of 15 consecutive patients who received a CPI model 0154 or 0155 active-fixation defibrillation electrode with an ICD system (CPI Ventak A V3DR model 1831 or CPI Ventak VR model 1774 defibrillator) are described. In 2 of the 15 patients, nonphysiological sensing appearing to be diaphragmatic myopotentials resulted in inappropriate defibrillator discharges. Both patients were pacemaker dependent. Changes in the sensitivity from nominal to less sensitive prevented inappropriate discharges. In one patient, discreet nonphysiological sensed events with the electrogram suggestive of ventricular activation was noted at the time of implantation. This was completely eliminated by redeployment of the active-fixation lead in the interventricular septum. In two other patients, discreet nonphysiological sensed events resulted in intermittent inhibition of ventricular pacing after implantation. These were still seen in the least sensitive autogain mode for ventricular amplitude. These were not seen on subsequent interrogation 1 month after implantation. Increased awareness of nonphysiological sensing is recommended. The CPI 0154 and 0155 leads seem to be particularly prone to this abnormality. Particular attention should be made when deploying an active-fixation screw for an integrated bipolar lead. This increased awareness is more important when a given individual is pacemaker dependent, which may warrant DFT testing in a least or less sensitive mode in these patients.

Adult↗
PubMed2000

Intradevice interaction in a dual chamber implantable cardioverter defibrillator preventing ventricular tachyarrhythmia detection.

Failure to detect ventricular tachycardia and/or ventricular fibrillation by implantable cardioverter defibrillators (ICDs) is a rare but serious problem. We report a case of failure to detect an episode of induced ventricular tachycardia by a dual chamber ICD, due to abbreviation of ventricular detection window secondary to programmed pacing parameters and a rate-smoothing algorithm. In this patient, the intradevice interaction was corrected by programming rate-smoothing off. This report highlights the potentially lethal consequences of critical timing relationships among the pacing function, arrhythmia detection, and the characteristics of the arrhythmia when using a modern dual chamber ICD. Physicians responsible for patients with ICDs must be aware of such interactions.

Algorithms↗
PubMed1998

Effects of propanolol in patients entered in the Beta-Blocker Heart Attack Trial with their first myocardial infarction and persistent electrocardiographic ST-segment depression.

OBJECTIVE/BACKGROUND: It has been shown that patients with an acute myocardial infarction and persistent electrocardiographic ST-segment depression are at high risk for subsequent cardiac events. The purpose of this retrospective analysis was to examine the long-term effects of propranolol therapy in patients with their first acute myocardial infarction and persistent electrocardiographic ST-segment depression. METHODS: The outcomes of 2877 patients enrolled in the Beta-Blocker Heart Attack Trial (BHAT) with their first myocardial infarction (75% of patients in BHAT) were reviewed. Patients were divided into three groups on the basis of presence or absence of > or =1 mm ST-segment depression in two contiguous leads of the 12-lead electrocardiogram obtained soon after admission or at the time of randomization, which occurred 10.1+/-3.5 days after the index myocardial infarction. Group 1 included 774 patients (392 randomly assigned to placebo and 382 to propranolol) with no ST-segment depression; group 2 included 1447 patients (713 placebo, 734 propranolol) with ST-segment depression at admission or at the time of randomization (labeled as transient); and group 3 included 656 patients (339 placebo and 317 propranolol) who had electrocardiographic ST-segment depression from the time of admission to the time of randomization (labeled as persistent). RESULTS: In group 3, patients with persistent electrocardiographic ST depression, the mortality rate in patients randomly assigned to placebo was 13.6% compared with 7.6% in patients with propranolol (p = 0.012; log rank test). Sudden death in the placebo arm was 9.7% compared with 4.7% in the propranolol group (p = 0.012, log rank test). The results of the Cox regression analysis, adjusting for all baseline variables with p values <0.25, showed the relative risk of overall mortality rate and the relative risk of sudden death were 2.13 ( 1.22, 3.70) and 2.56 (1.27, 5.26), respectively, for the placebo group compared with the propranolol group. Patients with persistent ST-segment depression had the greatest benefit from propranolol (47.2 fewer events [deaths/reinfarctions] per 1000 person-years compared with 78 and 2.1 fewer events in patients with transient and no ST-segment depression, respectively). CONCLUSIONS: It appears that the greatest benefit for beta-blocker therapy in patients after myocardial infarction is observed in patients with persistent ST-segment depression who are at greatest risk for death and reinfarction. Definitive conclusions regarding therapy with beta-adrenergic blocking agents in patients with persistent ST-segment depression cannot be made because our analysis, given its retrospective nature, is only hypothesis generating.

Adrenergic beta-Antagonists↗
PubMed1997

Mechanism of hypoxic K loss in rabbit ventricle.

Although a critical factor causing lethal ischemic ventricular arrhythmias, net cellular K loss during myocardial ischemia and hypoxia is poorly understood. We investigated whether selective activation of ATP-sensitive K (KATP) channels causes net cellular K loss by examining the effects of the KATP channel agonist cromakalim on unidirectional K efflux, total tissue K content, and action potential duration (APD) in isolated arterially perfused rabbit interventricular septa. Despite increasing unidirectional K efflux and shortening APD to a comparable degree as hypoxia, cromakalim failed to induce net tissue K loss, ruling out activation of KATP channels as the primary cause of hypoxic K loss. Next, we evaluated a novel hypothesis about the mechanism of hypoxic K loss, namely that net K loss is a passive reflection of intracellular Na gain during hypoxia or ischemia. When the major pathways promoting Na influx were inhibited, net K loss during hypoxia was almost completely eliminated. These findings show that altered Na fluxes are the primary cause of net K loss during hypoxia, and presumably also in ischemia. Given its previously defined role during hypoxia and ischemia in promoting intracellular Ca overload and reperfusion injury, this newly defined role of intracellular Na accumulation as a primary cause of cellular K loss identifies it as a central pathogenetic factor in these settings.

Action Potentials↗
PubMed1994

Effects of cyclic flexion of coronary arteries on progression of atherosclerosis.

The purpose of this investigation was to test the hypothesis that cyclic flexion of the coronary arteries contributes to the progression of atherosclerotic plaques. Coronary arteriograms were evaluated in 33 unselected patients who underwent 2 studies over a period of 25 +/- 16 months (mean +/- SD). Among the 33 patients, 103 plaques were identified. Plaques that showed progression were compared with plaques that showed no progression. The angle of flexion that occurred during systole at the site of the plaque was measured on the first arteriogram. In comparing progression versus no progression, the interval between arteriograms was 29 +/- 18 versus 23 +/- 14 months (p = NS) and percent stenosis at the first arteriogram was 42 +/- 28 versus 45 +/- 19% (p = NS). Percent stenosis at the time of the second arteriogram among plaques that progressed was 78 +/- 21%, and by definition, it remained 45 +/- 19% among those that did not progress. Among arteries with plaques that showed a progression of stenosis, the angle of flexion during systole was 19 +/- 13 degrees versus 9 +/- 15 degrees among arteries with plaques that did not progress (p < 0.01). Linear regression showed that the correlation of the angle of flexion with percent change of stenosis was relatively low (r = 0.32) but statistically significant (p < 0.005). Mathematic modeling of flexible and stiff plaques showed stresses approximately 1.5 to 1.9 times greater with 20 degrees than with 10 degrees flexion. Stresses due to flexion were usually greatest proximal and distal to the plaque along the subendothelial layer of the inner wall of the curved vessel. Data show that the angle of cyclic flexion, and consequently the stresses due to cyclic flexion of the artery were greatest in the region of plaques that progressed over the period of observation. Such stresses may have contributed to tissue damage of fatigue resulting in a more rapid progression of the atheromatous plaques.

Aged↗
PubMed1994

Chest radiographs fail to detect right ventricular enlargement and right atrial enlargement in patients with a pure restrictive ventilatory impairment.

The validity of measurements of the cardiac silhouette on chest radiographs for the evaluation of right ventricular enlargement and right atrial enlargement in patients with a pure restrictive ventilatory impairment was investigated in 19 patients. The forced vital capacity (FVC) percent predicted in these patients was 59 +/- 12 percent (mean +/- SD) (range, 29 to 79 percent). Right ventricular enlargement, by two-dimensional echocardiography, was defined as a right ventricular area > 20.4 cm2 and right atrial enlargement was defined as a right atrial area > 15.3 cm2. Chest radiographic measurements in the posteroanterior (PA) projection included distance from the midline to the farthest point of the right border of the cardiac silhouette, transverse cardiac diameter, and cardiothoracic ratio. Measurements in the lateral projection included the lateral horizontal transverse diameter, ventral portion of the lateral broad diameter, and obliteration of the retrosternal space. Neither the right ventricular area nor the right atrial area correlated with any of these radiographic measurements. There were no differences in these chest radiographic measurements among patients with normal right ventricular and right atrial dimensions, patients with right ventricular enlargement, and patients with right atrial enlargement. We conclude, therefore, that PA and lateral chest radiographs do not reliably detect right ventricular enlargement or right atrial enlargement in patients with a pure restrictive ventilatory impairment.

Cardiomegaly↗
PubMed1994

Right ventricular dilatation, right ventricular wall thickening, and Doppler evidence of pulmonary hypertension in patients with a pure restrictive ventilatory impairment.

The purpose of this investigation was to determine the severity of pure restrictive ventilatory impairment that results in right ventricular (RV) dilatation, increased RV wall thickness, and pulmonary hypertension. Two dimensional (2-D) echocardiography, Doppler measurements of pulmonary flow, and spirometry were performed on 26 unselected patients (17 female, 9 male) with a pure restrictive ventilatory impairment. A restrictive ventilatory impairment was defined as a forced vital capacity (FVC) < or = 80 percent predicted with a normal FEV1/FVC ratio (FEV1 = 1 s forced expiratory volume). The patients were grouped according to the severity of the restrictive ventilatory defect: mild (FVC, 65 to 80 percent predicted), moderate (FVC, 51 to 64 percent predicted), and severe (FVC < or = 50 percent predicted). An increased RV area (> 20.4 cm2) was shown in 0 of 10 (0 percent) patients with a mild impairment, 6 of 12 (50 percent) patients with moderate restriction, and 2 of 4 (50 percent) patients with severe restriction. Increased RV wall thickness (> 0.5 cm) was observed in 0 of 10 (0 percent) patients with mild restrictive impairment, 3 of 12 (25 percent) with moderate impairment, and 1 of 4 (25 percent) with severe restrictive impairment. Doppler evidence of pulmonary hypertension (ACT/ET ratio < 0.32) (ACT = acceleration time, ET = ejection time) was shown in 0 of 10 (0 percent) patients with a mild restrictive impairment, 8 of 12 (66 percent) patients with moderate restriction, and 4 of 4 (100 percent) patients with severe restriction (p < 0.01 mild vs moderate and mild vs severe). The RV area by 2-D echocardiography correlated well with the FVC percent predicted (r = 0.90, p < 0.001). The ACT/ET ratio also correlated well with the FVC percent predicted (r = 0.73, p < 0.001). In conclusion, RV enlargement and pulmonary hypertension were seen only in patients with a moderate or severe restrictive ventilatory impairment. These data may be useful in the assessment of the likelihood of subtle RV enlargement in patients with occupational pleuropulmonary disease.

Adult↗
PubMed1993

Prognostic significance of electrocardiographic persistent ST depression in patients with their first myocardial infarction in the placebo arm of the Beta-Blocker Heart Attack Trial.

The prognostic significance of ST segment depression in patients with their first acute myocardial infarction was investigated in 1444 patients with an acute myocardial infarction, who were randomly assigned to the placebo arm of the Beta-Blocker Heart Attack Trial (BHAT). Patients were divided retrospectively into three groups based on the presence or absence of > or = 1 mm ST segment depression in two contiguous leads of a 12-lead electrocardiogram obtained during the first few days after admission and at the time of randomization, which occurred at 9.7 +/- 3.3 days after the index myocardial infarction. Group 1 included 392 patients with no ST segment depression, group 2 comprised 713 patients with transient ST segment depression in the first few days after admission or at the time of randomization, and group 3 included 339 patients with persistent ST segment depression in the first few days after admission and at the time of randomization. At a median follow-up of 26 months, the mortality rate was 4.9% in group 1, 7.6% in group 2, and 13.6% in group 3. When Cox regression was used to adjust for baseline differences in other variables, the differences between the three groups continued to be highly significant (p = 0.005; 95% confidence intervals [0.6 and 1.4]). We conclude that persistent and transient ST segment depression in patients with their first myocardial infarction are strong predictors of increased long-term mortality when compared to patients without ST segment depression. These findings should be taken into consideration when stratifying patients at risk in the post-myocardial infarction period.

Electrocardiography↗
PubMed1993

Stratification of patients according to prior cardiopulmonary disease and probability assessment based on the number of mismatched segmental equivalent perfusion defects. Approaches to strengthen the diagnostic value of ventilation/perfusion lung scans in acute pulmonary embolism.

A categorical diagnosis of "high probability" or "intermediate probability" encompasses a spectrum of diagnostic probabilities of pulmonary embolism (PE) that is not communicated to the referring physician. The diagnostic value of ventilation/perfusion lung scans, in the present investigation, was strengthened by use of a table to determine the likelihood of PE in individual patients on the basis of the observed number of mismatched segmental equivalent perfusion defects. In addition, we tested the hypothesis that stratification of patients according to the presence or absence of prior cardiopulmonary disease may enhance the ventilation/perfusion scan assessment of the probability of PE among both of these clinical categories of patients. Data were derived from the collaborative study of the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED). Ventilation/perfusion lung scans were evaluated in 378 patients with acute PE and 672 patients in whom suspected PE was excluded. Among patients with no prior cardiopulmonary disease, > or = 1.0 mismatched segmental equivalents was indicative of PE in 102 of 118 (86 percent) vs 113 of 155 (73 percent) among patients with prior cardiopulmonary disease (p < 0.02). Among patients with prior cardiopulmonary disease, > or = 2 mismatched segmental equivalents were required to indicate > or = 80 percent probability of PE. Stratification on the basis of the presence or absence of prior cardiopulmonary disease, therefore, enhanced the ability of ventilation/perfusion scan readers to assign an accurate positive predictive value and specificity to individual patients based on the observed number of mismatched segmental equivalent defects. Among patients with no prior cardiopulmonary disease, fewer mismatched segmental equivalent defects were required to indicate a high probability of PE than were required by PIOPED criteria. The findings from some of these patients, by PIOPED criteria, would have indicated intermediate probability. Some indeterminate probability readings, therefore, will be eliminated among patients stratified with no prior cardiopulmonary disease.

Acute Disease↗
PubMedDate not supplied

Antithrombotic therapy in atrial fibrillation: a review of randomized trials with special reference to the Stroke Prevention in Atrial Fibrillation II (SPAF II) Trial.

Nonvalvular atrial fibrillation is common and is associated with a high risk of system embolism. Recently, several large randomized trials have been completed that have established the efficacy of antithrombotic therapy for both primary and secondary prevention of systemic thromboembolism with an acceptable rate of bleeding complications in these patients. This section of clinical trials review summarizes data from all published randomized trials of antithrombotic therapy in atrial fibrillation. The efficacy of aspirin versus warfarin is analyzed. The role of clinical and echo-cardiographic findings to stratify patients is also highlighted. The Stroke Prevention in Atrial Fibrillation II trial is discussed in detail.

Atrial Fibrillation↗