Biomedical subjects

B I Jugdutt

Publications and source records attributed to B I Jugdutt.

At least 73 records · Page 4Linked to original sources

PubMed1988

Effect of nitroglycerin and ibuprofen on left ventricular topography and rupture threshold during healing after myocardial infarction in the dog.

The effect of nitroglycerin and ibuprofen, given between 2 and 7 days after left anterior descending coronary artery ligation, on the mechanical resistance of the infarcted left ventricle to rupture or the rupture threshold (balloon technique), and on topography (computerized planimetry) and function (two-dimensional echocardiography) at 7 days (n = 32) and 42 days (n = 34) postligation was studied in 66 dogs randomly allocated to sham (no infarction, n = 22) and infarction subgroups (15 controls; 15 received nitroglycerin, 30 mg oral isosorbide dinitrate b.i.d.; 14 received ibuprofen, 200 mg t.i.d. orally). Nitroglycerin decreased mean arterial and left atrial pressures, decreased diastolic cross-sectional area, and improved systolic function, while ibuprofen increased diastolic area. Infarction subgroups showed infarct shrinkage and more infarct hydroxyproline at 6 weeks. Compared with shams, all infarct subgroups showed early expansion and thinning, with further marked late thinning in controls. Nitroglycerin produced less expansion and thinning both at 1 and 6 weeks, while ibuprofen produced marked early thinning. Rupture threshold was less at 6 weeks than 1 week with controls and ibuprofen but remained unchanged with nitroglycerin. Passive prerupture stiffness was less at 6 weeks than at 1 week in controls but remained unchanged with nitroglycerin and ibuprofen. Thus, reduced expansion and thinning with nitroglycerin during the first week after infarction improved function, mechanical strength, and resistance to distension at 6 weeks.

Animals↗

PubMed1988

Intravenous nitroglycerin therapy to limit myocardial infarct size, expansion, and complications. Effect of timing, dosage, and infarct location.

To determine 1) whether the effect of intravenous nitroglycerin (NG) therapy during acute myocardial infarction on creatine kinase infarct size is influenced by infarct location (anterior vs. inferior), timing (therapy less than 4 hours vs. greater than or equal to 4 hours after onset of pain), and dose response (mean blood pressure greater than or equal to 80 mm Hg vs. less than 80 mm Hg during the first 12 hours) and 2) whether NG therapy modifies infarct expansion, 310 patients were randomly allocated to NG (n = 154) and control (n = 156) groups. NG infusion was titrated to lower mean blood pressure by 10% in normotensive and 30% in hypertensive patients, but not below 80 mm Hg, and was maintained for 39 hours. Measurements included clinical variables, creatine kinase infarct size (geq) as well as left ventricular (LV) asynergy, LV ejection fraction, expansion index, and thinning ratio on serial two-dimensional echocardiography. Compared with controls, creatine kinase infarct size was less in the NG group (41 vs. 55 geq, p less than 0.001), in anterior (44 vs. 58 geq, p less than 0.05), and inferior (39 vs. 53 geq, p less than 0.025) NG subgroups, and in early than late NG subgroups (43% vs. 22% decrease). Other indexes of infarct size also improved (p less than or equal to 0.05) with NG compared with controls. Thus, by 10 days, LV asynergy was 40% less, LV ejection fraction was 22% more, and Killip class score was 41% less. A negative effect of mean blood pressure less than 80 mm Hg with NG was reflected in these indexes. In addition, expansion index increased (p less than 0.001) by 31% and thinning ratio decreased (p less than 0.001) by 17% in controls by 10 days but remained unchanged with NG. Infarct-related major complications were less frequent in the NG than the control groups: infarct expansion syndrome (2% vs. 15%, p less than 0.0005), LV thrombus (5% vs. 22%, p less than 0.0005), cardiogenic shock (5% vs. 15%, p less than 0.005), and infarct extension (11% vs. 22%, p less than 0.025). Mortality was less in NG than in control groups in-hospital (14% vs. 26%, p less than 0.01), at 3 months (16% vs. 28%, p less than 0.025) and 12 months (21% vs. 31%, p less than 0.05), but this advantage was only found in the anterior subgroups.(ABSTRACT TRUNCATED AT 250 WORDS)

Creatine Kinase↗

PubMed1987

Role of infarct expansion in rupture of the ventricular septum after acute myocardial infarction: a two-dimensional echocardiographic study.

To verify the role of infarct expansion (IE) in ventricular septal rupture (VSR) after transmural acute myocardial infarction (TAMI), topographic parameters were measured using tomographic imaging with two-dimensional echocardiography (2-D echo) and computer-aided analysis in four groups of patients: 8 patients with VSR (Group 1); 24 patients with TAMI but no mechanical complications (Group 2); 11 normal athletes (Group 3); 5 adults with congenital ventricular septal defect (Group 4). Measurements made on end-diastolic outlines of mid-left ventricular (LV) short-axis images included: LV asynergy (akinesis and/or dyskinesis), expansion index (asynergy/nonasynergy-containing endocardial segment length), thinning ratio (asynergic/nonasynergic wall thickness), and new indexes of regional shape distortion (RSD) by quantifying the deviation of the actual asynergic segment from the ideal asynergic arc constructed using the nearly circular nonasynergic contour. In Group 1, clinical IE (hypotension, congestive heart failure, no signs of new infarction) preceded detection of the VSR and portable 2-D echo showed the VSR associated with LV asynergy, marked IE, and RSD. Although Groups 1 and 2 had similar LV asynergy (28.7 vs. 26.9% LV) and ejection fraction (38.9 vs. 41.8%), Group 1 had higher expansion index (1.50 vs. 1.17, p less than 0.05), lower thinning ratio (0.54 vs. 0.67, p less than 0.005), and higher RSD parameters (e.g., peak distortion, Pk or maximum radial distance from the ideal arc, 19.3 vs. 3.9 mm, p less than 0.01; area of distortion, Ad, 7.4 vs. 1.1 cm2, p less than 0.05) than Group 2. Groups 3 and 4 had normal regional and global function and no evidence of expansion, thinning, or RSD. Thus, IE with marked diastolic RSD on an early 2-D echo after TAMI might identify patients at risk for VSR.

Aged↗

PubMed1987

Left ventricular catecholamines during acute myocardial infarction in the dog.

To determine whether changes in left ventricular catecholamine content occur during the first 30 to 90 min of acute myocardial infarction, myocardial catecholamine (radioenzymatic assay) over the interval was studied in the dog. In nine pentobarbital-anesthetized opened-chest dogs without coronary ligation, myocardial catecholamine at 2.5 h after pentobarbital (i) consisted mainly of norepinephrine (87% total catecholamine), (ii) showed a base to apex gradient in norepinephrine (1.44 +/- 0.10 vs. 1.03 +/- 0.10 micrograms/g, p less than 0.05) and dopamine (0.20 +/- 0.03 vs. 0.12 +/- 0.02 micrograms/g, p less than 0.05) but not epinephrine (0.017 vs. 0.016 micrograms/g), and (iii) showed no difference in norepinephrine, dopamine, or epinephrine across basal, mid, and apical left ventricular transverse planes spanning the vascular territories of the two coronary arteries. In 18 pentobarbital-anesthetized dogs with coronary ligation, (i) norepinephrine, measured in 14 regions across the mid left ventricle after 90 min ischemia in four dogs, was less in the ischemic center of the occluded bed than normal myocardium (1.01 +/- 0.04 vs. 1.29 +/- 0.04 micrograms/g, p less than 0.05), and (ii) norepinephrine was unchanged in normal myocardium of 14 dogs at 30, 60, 90 min, and 48 h but decreased in ischemic myocardium by 31% at 60 min (0.89 +/- 0.10 vs. 1.29 +/- 0.08 micrograms/g, p less than 0.025) and 79% at 48 h (0.27 +/- 0.04 vs. 1.26 +/- 0.08 micrograms/g, p less than 0.001). Thus, norepinephrine depletion from ischemic but not normal myocardium is detectable by 60 min during acute myocardial infarction.

Anesthesia↗

PubMed1987

Left ventricular rupture threshold during the healing phase after myocardial infarction in the dog.

The mechanical resistance of the infarcted left ventricle to rupture, or rupture threshold, was measured by the balloon technique 1-42 days after left anterior descending coronary artery ligation in 70 dogs: 26 without infarction (18 sham, 8 with ligation) and 44 with infarction. Rupture threshold in noninfarcted hearts was higher than in infarcted hearts (1168 +/- 165 (SD) vs. 754 +/- 223 mmHg (1 mmHg = 133.32 Pa), p less than 0.001) and did not change over 6 weeks. In contrast, rupture threshold in infarcted hearts decreased (p less than or equal to 0.05) after 14 days, the average value for 21-42 days being less than that for 1-14 days: 577 +/- 140 vs. 867 +/- 191 mmHg, p less than 0.001. Passive left ventricular stiffness in infarcted hearts was higher than for noninfarcted hearts throughout the 6 weeks during early filling (11.1 +/- 3.9 vs. 7.1 +/- 1.4 mmHg/mL, p less than 0.001) but decreased (p less than or equal to 0.05) after 14 days during the prerupture phase (11.3 +/- 5.3 vs. 6.2 +/- 3.0 mmHg/mL, p less than 0.005). Between 7 and 42 days, the infarct zone showed marked increase in hydroxyproline (10.0 +/- 2.0 vs. 48.8 +/- 19.7 mg/g dry weight, p less than 0.001), shrinkage (infarct size, 25 +/- 9 vs. 9 +/- 5% of the left ventricle, p less than 0.005), and thinning (infarct to normal wall thickness ratio, 0.83 +/- 0.11 vs. 0.51 +/- 0.09, p less than 0.001) but little further stretching (expansion index or the ratio of lengths of infarcted and noninfarcted segments, 1.14 +/- 0.10 vs. 1.28 +/- 0.17, p less than 0.2). A mild decrease (p less than 0.05) in left atrial pressure and increase (p less than 0.05) in diastolic area and fractional change in area (two-dimensional echocardiography) were detected at 6 weeks. The late decrease in rupture threshold and prerupture stiffness of the infarcted left ventricle and thinning of the scar suggest a late decrease in mechanical strength and resistance of the infarcted left ventricle to distension.

Animals↗

PubMed1987

Technetium pyrophosphate labelling following catheter shock: potential for a new intraoperative mapping technique.

Technetium pyrophosphate uptake at the site of catheter shock was studied in four patients and seven experimental dogs. Technetium pyrophosphate scintigraphy was performed following five catheter ablation attempts in humans at different cardiac sites, and following 24 J catheter shocks delivered in the right and left ventricles of seven dogs. In the patients, gamma camera imaging with tomographic reconstruction showed intense focal uptake at the sites of shock. The scans were positive from 1.5 to 5.5 h following ablation and stayed positive for up to five days. In the animals, the low energy shocks produced circumscribed areas of coagulation and contraction band necrosis. The binding of technetium pyrophosphate at these sites was confirmed by in vivo gamma camera imaging, epicardial counting with a 1.2 cm scintillation probe and ex vivo imaging. Ratios of focal binding to normal myocardial uptake of technetium pyrophosphate were calculated from the digital gamma camera images. In all cases, technetium pyrophosphate was bound to myocardial sites where transcatheter energies were delivered in both humans and dogs. Intraoperative localization of the origin of tachycardia in man may be facilitated by combining preoperative endocardial catheter mapping, catheter shock, radionuclide labelling of the site of shock and a search for the focus of radionuclide concentration during subsequent surgery.

Aged↗

PubMed1986

Increased myocardial infarct size by thiopental after coronary occlusion in the dog.

The effect of a single dose (10 mg/kg) of intravenous thiopental (TP), during acute myocardial infarction, on infarct size was studied in conscious dogs randomized 10 minutes after left circumflex coronary artery occlusion to either the TP group (n = 10) or a control group given 0.9% saline solution (n = 10). During the first hour following therapy, myocardial blood flow (microspheres), arterial pressure, left atrial pressure, and arterial blood gases were similar in the two groups, but the heart rate (140 +/- 3 vs 110 +/- 3 bpm; p less than 0.001) and rate-pressure product (15,090 vs 12,210 bpm X mm Hg; p less than 0.025) were greater in the TP group. Infarct size (planimetry) and occluded bed size (postmortem coronary arteriography) measured 2 days later revealed that: the slope of the relation between infarct and occluded bed mass, as a percentage of the left ventricle (% LV) was greater with TP than with saline solution (1.10 vs 0.61; p less than 0.001); excluding hearts (four TP and three saline solution) with small occluded beds (less than 22% LV), infarcts were also larger with TP (n = 6) than with saline solution (n = 7), both as a percentage of the left ventricle (26.4 vs 12.2%; p less than 0.02) or occluded bed (61.5 vs 28.9%; p less than 0.005); and transmural and endocardial extents of the infarcts on topographic maps were greater with TP than with saline solution. In 12 other conscious dogs, increasing the heart rate between 10 and 70 minutes after left circumflex coronary artery occlusion to the average rate of the TP group (140 bpm) by atrial pacing resulted in infarcts larger than those in control dogs but similar to those in the TP group. Thus, TP therapy after left circumflex occlusion increased infarct size in dogs. This effect appeared to be due mainly to the increased heart rate, probably via increased myocardial oxygen demands.

Animals↗

PubMed1986

Healing after myocardial infarction in the dog: changes in infarct hydroxyproline and topography.

Temporal changes in infarct collagen and left ventricular topography during healing after myocardial infarction were studied in 132 dogs with coronary artery ligation: 8 sham dogs and 13 with no infarction (controls) and 111 with infarction (3 at 1 day, 54 at 2 days, 25 at 7 days, 3 at 2 weeks, 9 at 4 weeks and 17 at 6 weeks). Myocardial hydroxyproline (a marker of collagen) was measured by spectrophotometry and pathologic infarct size, arteriographic occluded bed size and topography by computerized planimetry of weighed left ventricular rings. Over 6 weeks, hydroxyproline was unchanged in normal regions (average 4.20 mg/g dry weight) but increased progressively between 7 days and 6 weeks (9.94 versus 55.55 mg/g, p less than 0.001) in infarct zones. Progressive infarct contraction occurred over 6 weeks, with infarct size at 6 weeks being 40% less than at 2 days (9.7 versus 16.3% of the left ventricle, p less than 0.001), although total infarct hydroxyproline was directly related to infarct size at each time period (r = 0.73 to 0.81, p less than or equal to 0.05). Significant (p less than or equal to 0.05) left ventricular topographic changes in infarct hearts compared with control hearts included: 1) increase in cavity area (5.0 versus 3.9 cm2), endocardial circumference (8.8 versus 7.4 cm) and expansion index (infarct/normal endocardial segment length, 1.21 versus 1.02) by 7 days; and 2) decrease in thinning ratio (infarct/normal wall thickness, 0.71 versus 0.98) by 6 weeks. Also, compared with 2 day infarcts, by 6 weeks infarct area was decreased (1.8 versus 3.4 cm2) and the noninfarcted segment length increased (6.9 versus 5.4 cm). Changes in hydroxyproline and topography were similar for anterior (n = 54) and posterior (n = 57) infarcts. Thus, healing in canine infarcts is associated with cavity dilation and infarct expansion within 7 days followed by infarct contraction and thinning by 6 weeks, whereas collagen increases between 7 days and 6 weeks. Collagen deposition in expanded and thinned infarct segments explains the permanent regional shape distortion associated with ventricular aneurysms.

Animals↗

PubMed1986

Difference in the relation between infarct and occluded bed in pentobarbital-anesthetized and conscious dogs.

The relationship between myocardial infarct size (IS) and occluded bed size (OBS) in pentobarbital-anesthetized (A, n = 16) and conscious (C, n = 20) dog models were compared. IS and OBS (postmortem coronary arteriography) were measured by computerized planimetry of weighed left ventricular (LV) rings 7 days after permanent left anterior descending (LAD, n = 19) or circumflex (LC, n = 17) coronary artery occlusion. For both A and C groups, IS was directly related to OBS (p less than 0.001) and no infarcts developed for small occluded beds. For either LAD or LC subgroups, infarcts were larger in A than C dogs (49 +/- 18 vs. 30 +/- 19% OBS, p less than 0.025), with greater slope of the linear regression between IS and OBS (p less than 0.001) and less epicardial sparing on topographic mapping (p less than 0.05). Although postocclusion mean arterial and left atrial pressures were similar in A and C groups, heart rates were greater in the A dogs, both pre- (125 vs. 88 beats/min, p less than 0.001) and post-occlusion (151 vs. 108 beats/min, p less than 0.001). Endocardial flows (radioactive microspheres) in infarct centers and margins were less in A than C dogs. Also, endocardial/epicardial (endo/epi) flow ratios in all regions were less in A than C dogs, both pre- and post-occlusion. Increasing heart rate in 10 other C dogs with LAD occlusion to that of the A group (151 beats/min) by right ventricular pacing resulted in larger infarcts with greater slope of the linear regression and less endo/epi flow ratios, as in the A group.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗

PubMed1985

Cardiac amyloidosis: combined use of two-dimensional echocardiography and electrocardiography in noninvasive screening before biopsy.

Cardiac amyloidosis (CA) presenting with intractable congestive heart failure, electrocardiographic (ECG) normal or low voltage, and conduction or rhythm disturbances, is rapidly fatal. During life, CA often mimics other cardiomyopathies so that definitive diagnosis depends on demonstration of amyloid on myocardial biopsy. On two-dimensional echocardiography (2-D echo), nonspecific features, such as increased ventricular wall thicknesses, predominant diastolic dysfunction, and diffuse myocardial "sparkling," are consistently found in CA. The combined presence of these 2-D echo features and normal or low voltage on ECG is highly suggestive of CA, allows differentiation from other cardiomyopathies, and might be useful in noninvasive screening before myocardial biopsy.

Adult↗

PubMed1985

Different relations between infarct size and occluded bed size in barbiturate-anesthetized versus conscious dogs.

The relation between infarct size and occluded bed size in barbiturate-anesthetized (n = 32) and conscious (n = 34) dogs was compared using models of the left anterior descending (n = 43) and circumflex (n = 23) coronary arteries with 2 day old infarcts. Infarct and occluded bed (postmortem coronary arteriography) masses were measured by computerized planimetry of weighed left ventricular rings. For either type of occlusion, infarcts were larger in anesthetized than in conscious dogs (56 versus 33% occluded bed, p less than 0.001), with greater slopes of the linear regressions between infarct size and occluded bed size (p less than 0.001) and less epicardial sparing (p less than 0.05) on topographic mapping. Although arterial and left atrial pressures were similar in the two groups, heart rates were higher in the anesthetized dogs, both before (127 versus 88 beats/min, p less than 0.001) and after (151 versus 109 beats/min, p less than 0.001) occlusion. Myocardial blood flow distribution (radioactive microspheres, n = 33) favored the epicardium in anesthetized dogs, with lower endocardial-epicardial flow ratios pre- and postocclusion. Also, the level of total plasma catecholamines (radioenzymatic assay) was higher in barbiturate-anesthetized (n = 5) than in conscious (n = 5) dogs. Increasing the heart rate in conscious dogs (n = 18) to that of the anesthetized group (139 beats/min) by pacing produced larger infarcts and greater linear regression slopes, as seen in anesthetized dogs. Decreasing the heart rate in anesthetized dogs (n = 7) to that of the conscious group (98 beats/min) by sinoatrial node destruction and pacing resulted in smaller infarcts and lower linear regression slope, as seen in conscious dogs. Thus, the larger infarcts in barbiturate-anesthetized dogs appeared to be related mainly to the tachycardia, although transmural maldistribution of flow and increased circulating catecholamines might have contributed.

Analysis of Variance↗

PubMed1985

Omega iodo fatty acid scintigraphy--what are we measuring?

In an open chested dog model utilizing dual isotope techniques (125I heptadecanoic acid and 9, 10 3H palmitic acid), sequential myocardial biopsies were performed to: validate the scintigraphic background subtraction technique for the iodo fatty acid, compare the myocardial activity time course for the fatty acids and by TLC methods determine the chemical form of the myocardial activity and to study the influence of free iodide on the overall time-activity pattern. The findings supported the method of background subtraction and demonstrated a similar activity-time course for the two fatty acids. In spite of this, approximately 30% of the myocardial activity (125I) was in the form of free iodide which suggested that the rate of diffusion of iodide may be an important kinetic element in the system. Some differences in the lipid form of the radioactivity (3H, 125I) were noted.

Animals↗

PubMed1985

Delayed effects of early infarct-limiting therapies on healing after myocardial infarction.

The effect of early infarct-limiting therapy on the hydroxypyroline (OHP, a marker of collagen) content and topography of 7-day-old infarcts was studied in 76 conscious dogs (69 ligated; seven sham operated). Two hours after their left anterior descending coronary arteries were occluded, 69 dogs were randomly assigned to receive 6 hr intravenous infusions of saline (controls; n = 29), low-dose nitroglycerin (NG; n = 13), prostacyclin (PGI2; n = 14), or ibuprofen (IBU; n = 13). Regional OHP (mg/g dry weight) was measured by spectrophotometry, and size of infarction and topography were determined by computerized planimetry. Infarct size was less in the NG, PGI2, and IBU groups compared with that in the saline group, both when measured as a percent of the arteriographic occluded bed (p less than .001) and as a percent of the left ventricle (p less than .005). For each treatment group (1) the level of OHP was higher (p less than .001) in the region of infarction (saline group, 9.9 +/- 0.7 mg/g; NG group, 14.9 +/- 1.9 mg/g; PGI2 group, 12.9 +/- 0.9 mg/g; IBU group, 10.6 +/- 1.4 mg/g) than in normal zones (4.4 +/- 0.2 mg/g), with more (p less than .05) OHP in border than center regions, and (2) the total OHP in the infarct zone was linearly related to size of infarction as a percent of the left ventricle (r = .89 to .94). However, the slopes of regressions for the NG, PGI2, and IBU groups were greater (p less than .001) than the slope for the saline group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1984

Right ventricular infarction: two-dimensional echocardiographic evaluation.

Seventeen patients with predominant right ventricular infarction (RVMI) were studied with two-dimensional echocardiography (2DE). On initial 2DE all had abnormal wall motion (AWM), defined as akinesis plus dyskinesis, in the inferior right ventricle (RV), inferior interventricular septum, and inferior left ventricle (LV). The extent of RV vs LV AWM in short-axis sections at mitral, chordal, and papillary levels was 58% vs 29%, 56% vs 38%, and 59% vs 38%, respectively. The calculated topographic extent of AWM was greater in the RV than in the LV (58% vs 36%, p less than 0.05), and the RV/LV ratio (1.65) exceeded (p less than 0.001) unity. Peak creatine phosphokinase levels correlated significantly (p less than 0.001) with the topographic extent of LV AWM (r = 0.79) or RV + LV AWM (r = 0.75). Although all patients had RV dilatation, eight also had LV dilatation. Serial studies detected the cause of mechanical complications (n = 13), mural echo densities suggesting thrombi (LV in six and RV in seven), and persistent AWM in survivors. Thus, 2DE provided diagnostic data, and assessment of RV and LV AWM confirmed predominant RV involvement.

Adult↗

PubMed1984

Evaluation of biventricular involvement in hypotensive patients with transmural inferior infarction by two-dimensional echocardiography.

Hypotension in inferior myocardial infarction (IMI) may be due to extensive involvement of the right ventricle (RV), left ventricle (LV), or both. We verified this hypothesis in 24 patients with IMI and hypotension (systolic blood pressure less than 100 mm Hg), within 48 hours of admission, by means of two-dimensional echocardiography (2DE). We measured the extent of regional RV and LV asynergy (akinesis and/or dyskinesis) in parasternal short-axis sections at mitral, chordal, midpapillary muscle, and low papillary muscle levels. Initial right heart catheterization revealed predominant RV dysfunction in 16 patients (group 1) and predominant LV dysfunction in eight patients (group 2). For all patients, the initial 2DE revealed: (1) biventricular asynergy involving the posterior RV, posterior LV, and posterior interventricular septum; (2) a wide range of values for the extent of asynergy (RV 21% to 90%; LV 19% to 48%); and (3) a direct correlation between peak creatine kinase levels and percentage of LV asynergy (r = 0.80, p less than 0.001) or percentage of RV plus LV asynergy (r = 0.72, p less than 0.001). Although the extent of LV asynergy was similar in the two groups (34% vs 34%, NS), the extent of RV asynergy was greater in group 1 than in group 2 (57% vs 30%, p less than 0.001). More important, the ratio of RV/LV asynergy was greater for group 1 than group 2 (1.75 vs 0.89, p less than 0.001), and this difference in ratios between the two groups was also found in 2DE studies at 10 days and 6 months. A RV/LV asynergy ratio value of 1.1 provided clear separation between the groups. Thus, the RV/LV asynergy ratio on an initial 2DE can clarify the clinical syndrome of hypotension in patients with IMI. An increased asynergy ratio might identify those patients with predominant RV involvement.

Aged↗

PubMed1984

Inferior ST segment depression during acute anterior myocardial infarction: clinical and angiographic correlations.

This study was performed to determine whether inferior ST segment depression during early stages of acute transmural anterior myocardial infarction identifies patients with multivessel coronary artery disease and additional inferior ischemia. Coronary and left ventricular angiography were performed within 3.4 months in 33 patients with acute transmural anterior infarction. Initial electrocardiograms, 2 to 5 hours after onset of chest pain, revealed significant ST segment depression (greater than or equal to 0.1 mV) in at least two of leads II, III and a VF in 15 patients (45%) (group B); in 18 patients (group A) this finding was absent. Compared with group A, patients in group B had greater anterior ST elevation (1.2 versus 0.7 mV, p less than 0.025); higher serum peak creatine kinase (2,475 versus 1,147 IU/liter, p less than 0.005); higher Killip scores (2.1 versus 1.3, p less than 0.001); more in-hospital complications (60 versus 17%, p less than 0.05); lower mean left ventricular ejection fraction (34 versus 55%, p less than 0.001); more frequent regional left ventricular dysfunction in anterolateral (91 versus 44%, p less than 0.05), posterolateral (36 versus 0%, p less than 0.05) and inferior (100 versus 6%, p less than 0.005) regions; greater wall motion abnormality scores (10.0 versus 5.5, p less than 0.005); higher frequency of concomitant left circumflex or right coronary artery disease, or both (80 versus 28%, p less than 0.01); more frequent postinfarction angina (100 versus 39%, p less than 0.001) and lower New York Heart Association functional classification scores (1.7 versus 2.4, p less than 0.05) at 6 month follow-up. The time course of inferior ST depression differed from that of anterior ST elevation. Thus, inferior ST depression was maximal in the first 48 hours and decreased (p less than 0.05) thereafter. In contrast, ST elevation in leads V1 to V6 and I appeared to decrease (p = NS) between days 4 and 7. However, inferior ST depression "mirrored" ST elevation in lead aVL, which also decreased (p less than 0.05) after 48 hours. Thus, inferior ST depression during anterior infarction is associated with more extensive infarction, greater morbidity and higher frequency of multivessel coronary disease. Such inferior ST depression might reflect not only "reciprocal change," but also ischemia in adjacent lateral and remote inferior regions.

Adult↗

PubMed1983

Significance of precordial ST-segment depression in acute transmural inferior infarction: coronary angiographic findings.

Coronary arteriographic findings in patients with acute transmural inferior infarction were studied from 57 patients (51 men and 6 women). Their ages ranged from 28 to 72 years with a mean of 50 years. Twenty-six patients (Group A) had minimal (less than 0.1 mV) or no precordial ST-segment depression. Thirty-one patients (Group B) had precordial ST-segment depression of 0.1 mV or more. The two groups showed consistent differences in frequency of the left anterior descending artery (LAD) stenosis, multivessel disease, mean peak plasma creatinine phosphokinase (CPK, IU/L), and mean ejection fraction. For Group A vs B, these differences were: LAD stenosis, 31% vs 68%, multivessel disease, 35% vs 81%, mean peak plasma CPK, 1283 versus 1904, and mean ejection fraction, 60.5% vs 45.3%. The incidence of abnormal anterolateral and posterobasal wall motion in Group B was more (p less than 0.01 and p less than 0.05 respectively) than in Group A. All patients in Group B who had precordial ST-segment depression of 0.3 mV or greater, had LAD stenosis. There was no relation between the duration of ST-segment depression and the presence of LAD stenosis. Also, there was no correlation between the presence of collateral circulation and the development of ST-segment depression. The Group B patients tended to have more complications in the acute phase and in the follow up period (p less than 0.05) than did those in Group A. It is concluded that precordial ST-segment depression in acute inferior wall infarction is probably related to anterior injury due to LAD stenosis and these patients were shown to have more severe coronary artery disease, more depression of their ejection fractions, and more myocardial damage than patients without this finding. The earliest recorded ECG is most valuable in identifying the high risk patients. The presence of LAD stenosis in patients with inferior wall infarction who have precordial ST-segment depression of 0.3 mV or more are likely.

Adult↗

PubMed1983

The modern diagnosis of cardiac myxoma: role of two-dimensional echocardiography.

We reviewed our experience with the diagnosis of cardiac myxoma in 10 patients seen between 1960 and 1981. At surgery, large myxomas (greater than 5 cm) were found in the left atrium in 6 patients, right atrium in 3, and right ventricle in 1. The correct preoperative diagnosis was made in 9 patients: clinically in 3 and at catheterization and angiocardiography in 6. Diagnoses were falsely negative in 3/13 (23%) catheterizations and 2/10 (20%) angiocardiograms. Echocardiography (echo) was positive in 5/5 (100%). Gated blood-pool scans confirmed a right atrial myxoma in 1 patient. The interval between onset of symptoms and surgery was 30.5 months, (range, 2-120) and was not significantly different in the eras before and after echo. The age at diagnosis exceeded 40 years in 9 patients and was not significantly less in the echo era. The size and site of the tumor at surgery agreed with findings on M-mode echo (n=5) or two-dimensional (2-D) echo (n=2), but the size (85 vs. 88 cm3) and mass (81 vs. 88 g) of the tumors were similar in the 2 eras. Although 2-D echo facilitates the preoperative diagnosis of cardiac myxoma, earlier patient referral of suspicious cases for 2-D echo is still necessary.

Adult↗