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Biomedical subjects

V S Banka

Publications and source records attributed to V S Banka.

At least 37 records · Page 2Linked to original sources

Critical analysis of the application of Bayes' theorem to sequential testing in the noninvasive diagnosis of coronary artery disease.

The utility of Bayes' theorem in the noninvasive diagnosis of coronary artery disease (CAD) was analyzed in 147 patients who underwent electrocardiographic stress testing, thallium-201 perfusion imaging and coronary angiography. Eighty-nine patients had typical anginal chest discomfort and 58 had atypical chest pain. Sensitivity and specificity of the tests and prevalence of CAD at each level of testing were tabulated and compared with the results generated from Bayes' theorem. The sensitivity of electrocardiographic stress was higher in patients with multivessel CAD than in patients with 1-vessel CAD. Sensitivity, but not specificity, of each test was dependent, in part, on the result of the other test. However, the probabilities calculated from Bayes' theorem when used for sequential testing are remarkably close to the tabulated data. Thus, Bayes' theorem is useful clinically despite some evidence of test dependence. Sequential test analysis by Bayes' theorem is most useful in establishing or ruling out a diagnosis when the pretest prevalence is approximately 50% and when the 2 tests are concordant.

Aged↗

Variable effects of intracoronary nitroglycerin on myocardial blood flow and segmental shortening according to dose and degree of coronary occlusion.

The effects of intracoronary nitroglycerin were determined in 21 open-chest dogs. Six dogs with severe stenosis (25 mm Hg diastolic perfusion pressure) and nine dogs with moderate stenosis (40 mm Hg) received a 12 micrograms bolus followed by 44 micrograms/min intracoronary nitroglycerin. In addition, six dogs with moderate stenosis (40 mm Hg) received 5 micrograms followed by 5 micrograms/min nitroglycerin. Myocardial blood flow was measured with radioactive microspheres and segment shortening with ultrasonic crystals. At 40 mm Hg, high-dose but not low-dose nitroglycerin raised epicardial blood flow, while at 25 mm Hg nitroglycerin had no effect. Subendocardial blood flow was not affected in any group. Partial occlusion resulted in a decrease in segment shortening in the 25 mm Hg group but not at 40 mm Hg. High-dose nitroglycerin had no effect on shortening at either level of occlusion. Thus, in the presence of coronary vascular reserve, high-dose nitroglycerin may overcome coronary autoregulation. A dose equivalent to one that simulates the amount of nitroglycerin delivered to the coronary circulation by a systemic infusion did not affect myocardial blood flow. In addition, even a large dose of nitroglycerin did not affect segment shortening.

Animals↗

Quantitative thallium-201 imaging: limitations in detecting pathophysiologically significant obstructive coronary artery disease.

Washout of thallium-201 after stress testing has been proposed as a method of detecting abnormal zonal myocardial perfusion without relating it to a reference "normal" area. Therefore, 18 patients with single-vessel coronary artery disease, undergoing percutaneous transluminal coronary angioplasty, underwent maximum stress testing and thallium imaging. A myocardial perfusion defect was seen in the immediate postexercise images in all 19 zones (one patient studied twice) supplied by the vessel with the obstructive lesion. Delayed images showed improvement in 15 of the 19 segments. Of the four zones which did not improve, three had evidence of a prior nontransmural myocardial infarction. Quantitative analysis of washout curves showed that counts decreased in 17 of 19 zones after background subtraction and in all 19 zones if background was not subtracted. In the corresponding normal zones directionally similar decreases in counts were seen. Thus washout characteristics were similar for both diseased and normal zones. These data indicate that washout curves are limited in their ability to detect the presence of a physiologically significant lesion.

Adult↗

Influence of nifedipine on collateral blood flow during acute ischemia in the dog.

Vasodilators have been found effective in increasing blood flow in the lateral border surrounding a central zone of infarction, but any change in blood flow to this border zone may be to the normal tissue in this zone, rather than to the ischemic tissue. In this study of the effects of nifedipine on collateral blood flow, 31 open chest dogs underwent coronary occlusion followed by nifedipine infusion, either 3 or 1 microgram/kg per min. A balloon perfusion microsphere labeling device was used to separate the influence of normally perfused tissue overlapping with ischemic tissue in the lateral border zone. Nifedipine increased blood flow in the border zone, but this increase could be accounted for by the effect of nifedipine on admixed normal tissue. In the central ischemic zone, nifedipine administration resulted in a decrease in collateral blood flow. Thus, to fully understand the effect of a vasodilator on ischemic zone blood flow, it is necessary to account for flow in overlapping normal tissue.

Animals↗

Contrasting effects of nifedipine and verapamil on myocardium and vascular smooth muscle at two levels of coronary occlusion in the dog.

The calcium flux inhibitors nifedipine and verapamil have recently been used in the setting of both classical Heberden's and variant angina. It has also been suggested that these agents may preserve function and viability of threatened myocardium. The effects of these agents on the relationship between myocardial blood flow and contraction in the setting of partial coronary occlusion is unknown. Thus 39 open-chest dogs underwent partial coronary occlusion to diastolic perfusion pressures of 25 or 40 mm Hg. The dogs then received intracoronary infusions of 10 micrograms nifedipine or 100 micrograms verapamil. Myocardial blood flow was measured with tracer microspheres and myocardial shortening was assessed with ultrasonic crystals. At 25 mm Hg nifedipine improved myocardial shortening while blood flow did not change. In contrast, verapamil caused shortening to be abolished but also did not change blood flow. At 40 mm Hg nifedipine, while not affecting shortening, caused a "redistribution" of blood flow from endocardium to epicardium; in contrast, verapamil again caused shortening to be abolished, but only increased epicardial blood flow leaving endocardial flow intact. Thus verapamil and nifedipine have differing effects. Nifedipine is a potent vasodilator at doses having no negative inotropic effects. In addition, nifedipine can cause a transmural "redistribution" of blood flow from endocardium to epicardium. In contrast, verapamil is also a potent vasodilator, but has profound negative inotropic effects.

Animals↗

Comparative effects of nitroglycerin and nifedipine on myocardial blood flow and contraction during flow-limiting coronary stenosis in the dog.

Both nifedipine and nitroglycerin are used to treat angina pectoris. The comparative effects of these agents on myocardial blood flow and contraction in the setting of flow-limiting coronary stenosis are poorly understood. Thus 24 open chest dogs underwent carotid to left anterior descending coronary arterial perfusion with coronary flow probe and perfusion pressure monitoring. Segment length was measured with ultrasonic crystals in the subendocardial ischemic and nonischemic zones. Myocardial blood flow was measured with radioactive microspheres. Partial coronary occlusion was performed to attain a diastolic perfusion pressure of 40 mm Hg. Twelve dogs received intravenous nifedipine, 3 micrograms/kg per min, and 12 received intravenous nitroglycerin to reduce aortic pressure by 20 mm Hg. Partial occlusion resulted in a slight but significant decrease in segment shortening in the ischemic zone. Neither nitroglycerin nor nifedipine affected shortening in the ischemic zone. After occlusion, blood flow decreased in the subendocardial ischemic zone but was unchanged in the subepicardium. Nifedipine increased subendocardial blood flow in the nonischemic zone and decreased it in the ischemic zone but caused no change in subepicardial flow in the ischemic zone. In contrast, nitroglycerin decreased subendocardial and subepicardial blood flow in both the ischemic and nonischemic zones. In the setting of coronary stenosis, different classes of vasodilators may have varying effects on myocardial blood flow, suggesting different sites and mechanisms of action. In addition, segment function may not always reflect changes in myocardial blood flow.

Animals↗

Reversal of regional myocardial depressant effects of propranolol with nitroglycerin.

Use of propranolol in acute myocardial infarction is limited by its cardiodepressant effects. The effects of nitroglycerin (0.4 mg intravenously) on regional myocardial dysfunction produced by total or partial (50 percent) coronary occlusion and intravenous administration of propranolol (1.0 mg/kg) were evaluated using pairs of ultrasonic crystals implanted subendocardially in the nonischemic and ischemic zones in 14 open chest dogs. During partial coronary occlusion, systolic shortening (% delta L) in the ischemic zone decreased from 20.9 +/- 5.3 to 7.2 +/- 6.4 (p less than 0.001). Propranolol did not change it significantly. Nitroglycerin increased % delta L from 6.7 +/- 4.5 to 11.2 +/- 5.3 (p less than 0.01). The nonischemic zone was unaffected by partial coronary occlusion but showed a decrease in % delta L from 18.6 +/- 6.2 to 15.6 +/- 5.1 (p less than 0.01) with propranolol. Nitroglycerin increased % delta L from 15.6 +/- 5.1 to 17.3 +/- 5.9 (p less than 0.02). During total coronary occlusion, nitroglycerin administration after propranolol improved % delta L in the nonischemic but not in the ischemic zone. Nitroglycerin caused a significant decrease in left ventricular systolic and end-diastolic pressures. Heart rate remained unchanged. It is concluded that nitroglycerin reversed myocardial depressant effects of propranolol in both the partially ischemic and the nonischemic zones after acute coronary occlusion.

Animals↗

Contrasting ischemic contraction patterns by zone and layer in canine myocardium.

The effect of graded coronary occlusion on myocardial shortening in different zones of the left ventricle is not clear. Therefore, in 15 dogs ultrasonic crystals were used to evaluate the effect of graded coronary occlusion on subendocardial and subepicardial contraction in both the left anterior descending coronary artery (LAD) and left circumflex coronary artery (Circ) distributions. Subepicardial shortening was evaluated along both the long and short axes. In the LAD zones, segment shortening decreased in parallel in the subendocardium and subepicardium. In the circumflex zone subendocardial and subepicardial long axis shortening fell off in parallel, while subepicardial short axis shortening fell off more rapidly. Thus there is a close relationship between endocardial and epicardial segment shortening following graded coronary occlusion. In the circumflex zone, however, fiber orientation may affect the measurement of segment motion.

Animals↗

The effects of nifedipine on myocardial blood flow and contraction during ischemia in the dog.

Nifedipine has been proposed as an agent to preserve viability and function of ischemic myocardium. We studied 23 open-chest dogs that underwent carotid-to-left anterior coronary artery perfusion with flow probe and perfusion pressure monitoring. Segment length was measured with ultrasonic crystals in the ischemic and nonischemic endocardium. Myocardial blood flow was measured with radioactive microspheres. Partial coronary occlusion was performed to 25 mm Hg diastolic perfusion pressure. Ten dogs received intracoronary nifedipine, 10 micrograms, and 13 dogs received i.v. nifedipine, 3 micrograms/kg/min. Nifedipine resulted in an increase in segmental shortening in both groups, but nonischemic zone shortening did not change in either group. Nifedipine did not affect myocardial blood flow in the ischemic zone, but increased flow in the nonischemic zone in the group that received i.v. nifedipine. Thus, nifedipine appears to have a direct beneficial effect on ischemic myocardium.

Animals↗

Effects of digitalis on subendocardial and subepicardial dysfunction during acute ischemia.

The effects of digitalis (ouabain infusion, priming dose of 10 micrograms/kg/min followed by 2.0 micrograms/kg/min) on subepicardial and subendocardial ischemic dysfunction during partial occlusion (59.4% reduction in coronary flow) and total coronary occlusion were evaluated in 14 dogs using pairs of ultrasonic crystals implanted in the epicardial and endocardial layers. After 30 minutes of partial coronary occlusion, systolic shortening in the ischemic zone decreased from 12.4 +/- 2.9% to -0.4 +/- 0.9% (p less than 0.001) in the epicardium and from 18.9 +/- 3.1% to -1.0 +/- 1.1% (p less than 0.001) in the endocardium. Ouabain infusion increased the systolic shortening from -0.4 +/- 0.9% to 10.6 +/- 3.1% (p less than 0.001) in the epicardium and from -1.0 +/- 1.1% to 17.2 +/- 3.4% (p less than 0.001) in the endocardium. The end-diastolic length did not change. In contrast, after 30 minutes of total coronary occlusion, systolic shortening in both epicardial and endocardial layers was replaced by systolic lengthening and remained unaffected by ouabain infusion in both layers. Systolic shortening in the nonischemic epicardial and endocardial layers increased consistently. We conclude that ouabain improves the contractile function of both ischemic epicardial and endocardial layers layers after partial coronary occlusion and does not worsen subendocardial ischemic dysfunction. After total coronary occlusion, however, the contraction of the ischemic zone is unaffected by ouabain.

Animals↗

Effects of isolated interventricular septal ischemia on global and segmental function of the canine right and left ventricle.

The effects of isolated septal artery ligation wee studied in 17 dogs. Contraction of the interventricular septum (IVS) and the free walls of both ventricles was measured by implanting ultrasonic crystals. Global ventricular function was assessed by Starling function curves. Following septal artery ligation, IVS shortening was immediately replaced by systolic lengthening. Thirty minutes after septal artery ligation, the right ventricular (RV) stroke work (SW) was significantly depressed at end-diastolic pressure (EDP) of 8 and 8.5 mm Hg from control values of 7.6 +/- 0.4 and 8.6 +/- 0.6 gmM to 6.7 +/- 0.4 and 7.4 +/- 0.5gmM respectively. However, LVSW after septal artery ligation was similar to control values for EDP from 5 to 19 mm Hg. These changes were associated with unchanged RV free wall movement of 21 +/- 3% in the inflow region and 23 +/- 5% in the outflow region. LV free wall systolic shortening following septal artery ligation increased by 16 +/- 3%. It is concluded that canine septal artery ligation causes global dysfunction of the RV but not of the LV.

Animals↗

Differential effects of Renografin-76 on the ischemic and nonischemic myocardium.

The effects of intracoronary diatrizoate meglumine and diatrizoate sodium (Renografin-76) on regional contraction were examined in the normal coronary circulation and during partial (50 percent) coronary occlusion in 11 dogs using strain and length gauges. Intracoronary injections of Renografin-76 (1.5 cc) (1.690 mosM/liter; 0.19 mEq Na/ml), equiosmolar dextrose solution and 0.19 mEq Na+/ml saline solution were made randomly. Renografin-76 caused a decrease in preejection tension to 87.4 +/- 4.3 percent (p less than 0.025), total tension to 74.6 +/- 3.3 percent (p less than 0.01) and ejection tension to 11.9 +/- 12.6 percent (p less than 0.001) of control value. Segment length increased to 106.7 +/- 7.3 percent of control value. These changes lasted only 12 +/- 2 (range 5 to 20) seconds (mean +/- standard error of the mean). During partial coronary occlusion and after injection of Renografin-76, preejection tension decreased from 91.7 +/- 6.3 to 53.8 +/- 3.9 percent (p less than 0.01), total tension from 89.9 +/- 5.0 to 59.7 +/- 3.5 percent (p less than 0.01) and ejection tension from 22.8 +/- 8.1 to 17.8 +/- 10.9 percent, whereas segment length increased from 112.7 +/- 3.7 to 130.7 +/- 4.6 percent (p less than 0.01) of control value. In contrast to findings in the normal coronary circulation, tension and length changes lasted 54 +/- 16 (range 15 to 180) seconds (p less than 0.05). The hyperemic response during normal coronary circulation was completely abolished during partial coronary occlusion. Prior administration of nitroglycerin did not shorten the duration of the myocardial depressant effects of Renografin. Injections of equiosmolar dextrose or saline solution produced qualitatively similar but quantitatively less marked changes. Thus, intracoronary Renografin-76 has an accentuated and prolonged depressant effect on the ischemic as compared with the normally perfused myocardium; this effect is not solely due to its hyperosmolarity or sodium concentration.

Animals↗

Natural history of contractile abnormalities after acute myocardial infarction in man: severity and response to nitroglycerin as a function of time.

The natural history of contraction abnormalities and their response after acute myocardial infarction in man were studied using radionuclide angiography. Sixteen patients were studied before and after sublingual nitroglycerin within 24 hours, 5-7 days and 4-6 weeks after the onset of chest pain. Within 24 hours, central chord shortening in the zone of infarction was reduced to 13.1 +/- 9.8%, but improved 27.2 +/- 18.4% (p less than 0.001) after nitroglycerin. After 5-7 days, central chord shortening improved similarly, but less markedly, from 12.9 +/- 9.2% to 24.4 +/- 13.2% (p less than 0.001). After nitroglycerin 4--6 weeks after the acute myocardial infarction, the central chord showed no response to nitroglycerin; it was 13.9 +/- 10.9% before and 13.4 +/- 2.5% after nitroglycerin. Changes in the lateral chords paralleled changes in the central chords in the three studies. Nonischemic zone improvement after nitroglycerin in all three studies. Global ejection fraction improved and end-diastolic and end-systolic volumes decreased in all three studies after nitroglycerin. These data indicate that after acute myocardial infarction, there is a significant reduction in hemiaxis shortening in the central and lateral chords that remains essentially unchanged over 4-6 weeks. However, the asynergic ischemic area improves considerably after nitroglycerin within 24 hours and 5-7 days, but fails to improve after 6 weeks.

Acute Disease↗

Interventricular septal motion: biventricular angiographic assessment of its relative contribution to left and right ventricular contraction.

The interventricular septum (IVS) has conventionally been regarded as a functional part of the left ventricle (LV). To determine its normal range of motion, simultaneous biventricular cineangiograms (60 frames/sec) were performed (60 degrees left anterior oblique) in nine subjects without coronary or other heart disease. Arrhythmias were avoided by using a specially designed right ventricular (RV) angiographic catheter. IVS motion was studied qualitatively by three observers and quantitatively by superimposing end-systolic and diastolic frames using intra- and extracardiac reference points. Two transverse chords that trisected the end-systolic length of the IVS were drawn to quantitate IVS, LV and RV free wall motion. Qualitatively, the IVS thickened toward both RV and LV cavities as a result of shortening on its longitudinal axis. LV motion was 39.9 +/- 7.2% on the transverse axis, of which 31.2 +/- 5.2% was contributed by the LV free wall and 8.5 +/- 2.1% by IVS. RV transverse axis motion was 36.9 +/- 3.7%, of which 28.6 +/- 2.1% was contributed by the RV free wall and 8.3 +/- 2.3% by IVS motion. There was no difference between IVS motion toward the LV and that toward the RV. The IVS longitudinal axis shortened by 17.4 +/- 2.8% (p less than 0.001). The mean systolic IVS thickness increased symmetrically from 7.43 +/- 0.55 mm to 12.49 +/- 0.39 mm (p less than 0.001). In brief, the IVS thickens on its transverse axis and shortens on its longitudinal axis, contributing equally to RV and LV function.

Adult↗

The relationship between myocardial blood flow and contraction by myocardial layer in the canine left ventricle during ischemia.

We investigated the relationship between regional myocardial blood flow (MBF) and segmental shortening in 17 open-chest dogs. The left anterior descending coronary artery was cannulated and perfused from the left carotid while measuring perfusion pressure. Graded occlusion was produced by a screw clamp. Extent of occlusion was monitored by perfusion pressure. Percent systolic shortening (% delta L) was measured using ultrasonic crystals implanted in normal and ischemic endocardium and ischemic epicardium. MBF was measured in ischemic and normal endocardium and epicardium with tracer microspheres. Dogs underwent 1 to 4 grades of coronary stenosis. Myocardial blood flow both to endocardium and epicardium was found to be linearly related to diastolic perfusion pressure below 50 mmHg (r = 0.803 and 0.748, respectively). Normalized % delta L (N% delta L) was best related to fraction normal zone MBF in the endocardium by the sigmoidal equation, N% delta L = e9.01 MBF-4.03/1 + e9.01 MBF-4.03. % delta L was only weakly related to myocardial blood flow in the epicardium (r = 0.584), and, in four dogs, % delta L was zero in the epicardium despite normal regional blood flow. However, % delta L in the epicardium was linearly related to % delta L in the endocardium (r = 0.78). Thus, endocardial wall motion is related to MBF by a sigmoidal relationship while epicardial wall motion is tethered to endocardial wall motion.

Animals↗

Variable effect of nifedipine on myocardial blood flow at three grades of coronary occlusion in the dog.

The effect of nifedipine on myocardial blood flow at various grades of coronary stenosis is unknown, Thus 22 open-chest dogs underwent carotid to left anterior descending perfusion with flow and perfusion pressure monitoring. Grades of coronary occlusion were defined by minimum diastolic perfusion pressure. six dogs (group 1) underwent moderate occlusion to 50 to 55 mm Hg diastolic perfusion pressure; (group 2), severe occlusion to 40 mm Hg perfusion pressure; and six (group 3), more severe occlusion at 25 mm Hg. Regional myocardial blood flow was measured with radioactive microspheres before and after the intracoronary injection of 10 microgram of nifedipine. In group 1, nifedipine induced epicardial hyperemia and little change in endocardial flow in the ischemic zone. In group 2, nifedipine induced epicardial hyperemia from 1.06 to 1.39 mg/g per min, but endocardial flow decreased from 0.70 to 0.60 ml/g per min. In group 3, there was no change in blood flow. Thus the effect of nifedipine on myocardial blood flow depends on the extent of occlusion. Furthermore for certain degrees of occlusion, redistribution of blood flow from endocardium to epicardium has been shown to occur.

Animals↗