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Background & Aims: Patients with cirrhosis and significant coronary artery disease (CAD) are at risk of peri-liver transplantation (LT) cardiac events. The coronary artery disease in liver transplantation (CAD-LT) score and algorithm aim to predict the risk of significant CAD in LT candidates and guide pre-LT cardiac evaluation., Methods: Patients who underwent pre-LT evaluation at Indiana University (2010-2019) were studied retrospectively. Stress echocardiography (SE) and cardiac catheterization (CATH) reports were reviewed. CATH was performed for predefined CAD risk factors, irrespective of normal SE. Significant CAD was defined as CAD requiring percutaneous or surgical intervention. A multivariate regression model was constructed to assess risk factors. Receiver-operating curve analysis was used to compute a point-based risk score and a stratified testing algorithm., Results: A total of 1,771 pre-LT patients underwent cardiac evaluation, including results from 1,634 SE and 1,266 CATH assessments. Risk-adjusted predictors of significant CAD at CATH were older age (adjusted odds ratio 1.05; 95% CI 1.03-1.08), male sex (1.69; 1.16-2.50), diabetes (1.57; 1.12-2.22), hypertension (1.61; 1.14-2.28), tobacco use (pack years) (1.01; 1.00-1.02), family history of CAD (1.63; 1.16-2.28), and personal history of CAD (6.55; 4.33-9.90). The CAD-LT score stratified significant CAD risk as low (≤2%), intermediate (3% to 9%), and high (≥10%). Among patients who underwent CATH, a risk-based testing algorithm (low: no testing; intermediate: non-invasive testing vs. CATH; high: CATH) would have identified 97% of all significant CAD and potentially avoided unnecessary testing (669 SE [57%] and 561 CATH [44%])., Conclusions: The CAD-LT score and algorithm (available at www.cad-lt.com) effectively stratify pre-LT risk for significant CAD. This may guide more targeted testing of candidates with fewer tests and faster time to waitlist., Lay Summary: The coronary artery disease in liver transplantation (CAD-LT) score and algorithm effectively stratify patients based on their risk of significant coronary artery disease. The CAD-LT algorithm can be used to guide a more targeted cardiac evaluation prior to liver transplantation., Competing Interests: Conflict of interest The authors declare no conflicts of interest that pertain to this work. Please refer to the accompanying ICMJE disclosure forms for further details., (Copyright © 2021 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.)

Background and Aims: A study at Indiana University demonstrated a reduction in myocardial infarction (MI) incidence with increased frequency of cardiac catheterization (CATH) in liver transplant (LT) candidates. A strict protocol for performing CATH based upon predefined risk factors, rather than noninvasive testing alone, was applied to a subgroup (2009-2010) from that study. CATH was followed by percutaneous coronary intervention (PCI) in cases of significant coronary artery disease (CAD; ≥50% stenosis). The current study applies this screening protocol to a larger cohort (2010-2016) to assess post-LT clinical outcomes., Approach and Results: Among 811 LT patients, 766 underwent stress testing (94%) and 559 underwent CATH (69%), of whom 10% had CAD requiring PCI. The sensitivity of stress echocardiography in detecting significant CAD was 37%. Predictors of PCI included increasing age, male gender, and personal history of CAD (P < 0.05 for all). Compared to patients who had no CATH, patients who underwent CATH had higher mortality (P = 0.07), and the hazard rates (HR) for mortality increased with CAD severity (normal CATH, HR, 1.35; 95% confidence interval [CI], 0.79-2.33; P = 0.298; nonobstructive CAD, HR, 1.53; 95% CI, 0.84-2.77; P = 0.161; and significant CAD, HR, 1.96; 95% CI, 0.93-4.15; P = 0.080). Post-LT outcomes were compared to the 2009-2010 subgroup from the previous study and showed similar 1-year overall mortality (8% and 6%, P = 0.48), 1-year MI incidence (<1% and <1%, P = 0.8), and MI deaths as a portion of all deaths (3% and 9%, P = 0.35)., Conclusions: Stress echocardiography alone is not reliable in screening LT patients for CAD. Aggressive CAD screening with CATH is associated with low rate of MI and cardiac mortality and validates the previously published protocol when extrapolated over a larger sample and longer follow-up period., (© 2019 American Association for the Study of Liver Diseases.)

Postoperative atrial fibrillation/flutter (POAF) is the most common perioperative arrhythmia and may be particularly problematic after liver transplantation (LT). This study is a single-center retrospective analysis of POAF to determine its incidence following LT, to identify risk factors, to assess its impact on clinical outcomes, and to summarize management strategies. The records of all patients who underwent LT between 2010 and 2018 were reviewed. Extracted data included pre-LT demographics and cardiac evaluation, in-hospital post-LT cardiac events, early and late complications, and survival. Among 1011 patients, the incidence of post-LT POAF was 10%. Using binary logistic regression, pre-LT history of atrial fibrillation was the strongest predictor of POAF (odds ratio [OR], 6.72; 95% confidence interval [CI], 2.00-22.57; P < 0.001), followed by history of coronary artery disease (CAD; OR, 2.52; 95% CI, 1.10-5.81; P = 0.03). Cardiac stress testing abnormality and CAD on cardiac catheterization were also associated with higher risk. Median time to POAF onset after LT was 3 days with 72% of cases resolving within 48 hours. POAF patients had greater hospital length of stay, death during the LT admission, and 90-day and 1-year mortality. POAF was an independent risk factor for post-LT mortality (OR, 2.0; 95% CI, 1.3-3.0; P < 0.01). Amiodarone was administered to 73% of POAF patients with no evidence of increased serum alanine aminotransferase levels. POAF occurred in 10% of post-LT patients with early onset and rapid resolution in most affected patients. POAF patients, however, had significant morbidity and mortality, suggesting that POAF is an important marker for worse early and late post-LT outcomes., (Copyright © 2019 by the American Association for the Study of Liver Diseases.)

Limited data regarding the optimal risk assessment strategy for evaluating candidates for orthotopic liver transplantation (OLT) exist. Our center has adopted a policy of performing cardiac catheterization (CATH) in patients with predefined risk factors, and this is followed by percutaneous coronary intervention (PCI) when it is indicated, even in the presence of negative stress test findings. The aim of this single-center, retrospective study of all patients who underwent OLT between 2000 and 2010 was to assess the effect of our policy on cardiovascular (CV) complications and survival rates after OLT. Data, including 1-year all-cause and CV mortality, postoperative myocardial infarctions (MIs), and frequencies of CATH and PCI, were abstracted. The study was divided into 3 subperiods to reflect the changes in policy over this period: (A) 2000-2004, (B) 2005-2008, and (C) 2009-2010. One thousand two hundred twenty-one patients underwent OLT between 2000 and 2010. The rate of catheterization increased during the 3 time periods (P < 0.001), as did the rate of PCI (P < 0.05). All-cause mortality decreased over the periods (P < 0.001), as did the MI rate (P < 0.001). Thirty-five of the 57 patients requiring PCI had normal stress tests. The mortality rate associated with postoperative MIs was significantly higher than the overall all-cause mortality rate. In conclusion, a significant improvement in the overall survival rate over the 3 analyzed time periods was noted. Increases in the frequencies of CATH and PCI corresponded to significant reductions in postoperative MIs and 1-year all-cause mortality rates. The increased use of CATH and PCI was associated with reduced overall all-cause mortality through reductions in the incidence of both fatal and nonfatal MIs. Further analyses of the role of stress testing and CATH in evaluating and treating patients before OLT are required to optimize this process., (© 2014 American Association for the Study of Liver Diseases.)

Background: Assessment of viability of myocardium after an ischemic insult is an important clinical question that affects decisions pertaining to potential revascularization. The results of contrast left ventriculograms and coronary angiography were compared to positron emission tomography (PET) in 64 patients with coronary artery disease and reduced left ventricular function., Hypothesis: The study was undertaken to determine the relative utility of the invasive studies in the assessment of viability., Methods: Right anterior oblique ventriculograms were assessed for hypokinesis, akinesis, or dyskinesis in six segments. The PET scans were assessed for viability by visual estimation of flourodeoxyglucose (FDG) uptake in six segments that corresponded to the segments analyzed on the ventriculograms., Results: Of a total of 373 segments successfully analyzed by PET, 272 were judged to be viable (normal or hypokinetic) by contrast ventriculography. Of these, 253 (93%) were considered viable by PET. Of 177 segments deemed either normal or mild-to-moderately hypokinetic by ventriculography, 170 (94%) were viable by PET. Of 95 severely hypokinetic segments, 83 (84%) were viable by PET. Of 79 akinetic segments, 44 (56%) were considered viable by PET. For segments that were dyskinetic and thought to be nonviable by ventriculography, 19 of 22 (86%) were also considered nonviable by PET. For 294 segments for which a determination on viability was made based on the presence of wall motion on the ventriculogram (normal, hypokinetic, ordyskinetic; not akinetic), there was excellent agreement with PET (93%; p < 0.001). In 49 patients there was akinesis in no more than one segment in either the anterior or inferior territories, indicating the potential for assessment of viability by ventriculography in at least two of three segments in each territory. Coronary anatomy was analyzed to assess whether coronary patency could help in assessing viability. Segments supplied by patent arteries were more likely to be viable by PET than segments supplied by occluded arteries (p < 0.001). Akinetic segments were more likely to be supplied by occluded arteries (56 vs. 23, 72%). Dyskinetic segments were predominantly nonviable by PET (86%) and were usually supplied by occluded arteries (77%)., Conclusion: In patients in whom the assessment of viability is clinically relevant, the presence of systolic inward motion on the contrast left ventriculogram correlates well with segment viability by PET, while outward or dyskinetic movement correlates well with nonviability. Thus, the use of PET to assess viability in many patients may be unnecessary.

Devices to prevent distal atheroembolization are an important addition to the armamentarium of an interventional cardiologist. We report the use of PercuSurge, a distal balloon occlusion device, in two patients with recent myocardial infarction of differing etiologies. The first case is a patient with an old degenerated vein graft with thrombotic occlusion of greater than 48-hr duration and the second case is a patient with an embolic myocardial infarction in a native coronary artery. In both cases, significant thromboembolic debris was aspirated with technical success and no complications. These cases illustrate use of the PercuSurge device in patients after a recent myocardial infarction for preserving distal myocardial perfusion and microvascular integrity., (Copyright 2002 Wiley-Liss, Inc.)

Objectives: We investigated the patterns of perfusion and metabolism in dysfunctional myocardium whose contractility improved with dobutamine., Background: Clinical studies have suggested that dobutamine echocardiography can identify hibernating myocardium, but laboratory studies suggest that reduced perfusion limits the response to dobutamine., Methods: Twenty-five patients with coronary disease and ventricular dysfunction underwent low (5 and 10 micrograms/kg body weight per min) and high dose (maximum of 50 micrograms/kg per min) dobutamine echocardiography and positron emission tomography (PET) using nitrogen-13 (N-13) ammonia and fluorine-18 fluorodeoxyglucose (FDG) for imaging of perfusion and metabolism. Wall motion and tracer uptake were scored in 16 left ventricular segments., Results: Perfusion and metabolism were normal in 56.4%, mildly reduced in 29.1% and mismatched (reduced perfusion, preserved FDG uptake) in 14.5% of dysfunctional segments viable on PET. Wall motion improved with dobutamine in 89 dysfunctional segments (62 at low dose, 27 only at peak dose), and 86 of these (97%) were viable on PET. Improvement in wall motion with dobutamine was more common in segments with normal perfusion and metabolism (56.5%) than in those with mildly reduced tracer uptake (28.5%, p < 0.001) and those with mismatch (32%, p = 0.03). All the segments with a biphasic response were supplied by vessels with > or = 70% stenosis, and 88% had normal perfusion and metabolism., Conclusions: The majority of viable segments with rest dysfunction had normal perfusion and metabolism, suggesting that myocardial stunning was common. Improvement of wall motion at low and high doses of dobutamine was highly correlated with myocardial viability on PET and was more common in myocardium with normal perfusion. A biphasic response to dobutamine identified segments with normal perfusion and metabolism supplied by severely diseased vessels.

Fifty-one consecutive patients underwent exercise echocardiography, angiography, and intracoronary ultrasound (ICUS) 2.5 years (range from 1 to 6) after cardiac transplantation. The average age of the donor was 29 years (range 13 to 50), and the average age of the recipient was 49 +/- 12 years. In total, 78 studies were performed, as 25 patients had >1 annual evaluation and 2 patients had 3 consecutive annual evaluations. Of the 78 angiographic studies, 40 (26 patients) had evidence of coronary artery disease, defined as a focal stenosis (>20%, n=4) or luminal irregularities (n=36). However, by ICUS all 51 patients had intimal thickening at some point, with 34 patients possessing diffuse disease and 17 focal intimal thickening only. Of the 25 serial studies, 12 progressed by at least 1 Stanford class. The sensitivity of angiography for determination of class III to IV intimal thickening was 64% and the specificity was 76%. On exercise echocardiography, 6 examinations revealed resting wall motions abnormalities, whereas 6 had inducible wall motion abnormalities with exercise. The sensitivity of exercise echocardiography to determine class III to IV intimal thickening was 15%, and the specificity was 85%. In conclusion, exercise echocardiography is an insensitive method for predicting transplant-mediated coronary artery disease, whereas luminal irregularities on angiography may predict the presence of Stanford grade III to IV intimal thickening.

A 69-year-old man diagnosed with lung cancer had a transesophageal echocardiogram performed because of suspicion of intramyocardial tumor. The transesophageal echocardiogram confirmed the presence of both a right and left atrial mass. The lung cancer was believed to be potentially resectable if this mass did not represent tumor; therefore, biopsy of the intracardiac mass was requested. Intracardiac ultrasound was used to guide the biopsy procedure. Using intracardiac ultrasound guidance, a successful biopsy was performed that revealed the presence of tumor cells.

A modification of a previously described double balloon mitral valvuloplasty procedure is described. This involves dual femoral vein punctures with a single atrial septal puncture. After initial transseptal catheterization and predilatation of the interatrial septum with an 8-mm balloon, a second catheter is advanced through the resulting atrial septal defect allowing access to the left atrium and left ventricle through the mitral valve via two separate femoral vein puncture sites. In comparison with the previously described technique using two balloon catheters inserted through a single femoral vein puncture site, this modification has reduced the amount of bleeding from the femoral vein and the need for transfusion. Furthermore, the potential for subsequent interatrial shunting is less than with the alternative previously described technique utilizing two femoral vein punctures with two separate punctures in the interatrial septum. In utilizing two separate femoral vein punctures with only one atrial septal puncture this technique combines advantages of the two previously described techniques.

Background: Dysfunction after thrombolytic therapy of acute myocardial infarction (MI) may be reversible. Early after myocardial infarction, both reversible and irreversible injury may be manifested by regional wall motion abnormalities. Improved wall thickening during dobutamine infusion (dobutamine-responsive wall motion) may accurately identify reversibly injured segments., Methods and Results: To determine whether dobutamine-responsive wall motion accurately detects reversible postischemic dysfunction irrespective of infarct location, multistage (baseline, 4 and 12 micrograms.kg-1.min-1, and peak) dobutamine echocardiography (DE) was performed within 7 days of thrombolytic therapy. Resting echocardiography was repeated > or = 4 weeks after MI, and reversible dysfunction was defined as improved wall motion. The accuracy of dobutamine-responsive wall motion was compared with that of signs of early reperfusion, non-Q-wave MI, and peak creatine kinase (CK). Sixty-three patients underwent DE without complications. Follow-up echocardiograms were done in 51 (81%) of these patients, and wall motion improved in 22 (41%). Dobutamine-responsive wall motion during all stages of DE was very specific for reversible dysfunction (90% to 93%) but sensitive (86%) only when hemodynamics were not altered (low dose, 4 micrograms.kg-1.min-1). Non-Q-wave MI and a low peak CK (< 1000 IU/mL) were also specific (89% to 93%) but less sensitive (64% [P = .16] and 55% [P < .05], respectively). Signs of early reperfusion did not identify postischemic dysfunction. Low-dose dobutamine-responsive wall motion and non-Q-wave MI independently identified reversible dysfunction, but only dobutamine-responsive wall motion was sensitive in all infarct locations. Non-Q-wave MI was sensitive only in anterior infarction., Conclusions: Multistage dobutamine echocardiography can be performed safely early after thrombolytic therapy. Low-dose dobutamine-responsive wall motion accurately detected reversible dysfunction in all infarct locations. Dobutamine-responsive wall motion and non-Q-wave infarction may be very useful for accurately identifying reversible dysfunction early after thrombolytic therapy for acute MI.

Objectives: We examined the relation between the level of urinary fibrinopeptide A and the presence of angiographic intracoronary thrombus in patients with unstable angina to determine whether this marker predicts active thrombus formation., Background: Although it is known that thrombus plays a role in acute ischemic syndromes, a noninvasive method to predict its presence in individual patients with unstable angina has not been determined. Fibrinopeptide A is a polypeptide cleaved from fibrinogen by thrombin and thus is a sensitive marker of thrombin activity and fibrin generation., Methods: Angiographic thrombus, graded 0 to 4, and the presence of ST segment depression or T wave inversions, or both, on the electrocardiogram (ECG) were related to fibrinopeptide A levels in 24 patients with rest angina of new onset, 18 with crescendo angina, 19 with stable angina and 9 with chest pain but without coronary artery disease. All patients had chest pain within the 24 h of sample acquisition., Results: The angiographic incidence of thrombus was significantly higher in patients with new onset of rest angina (67%, p < 0.001) and crescendo angina (50%, p < 0.001) as were fibrinopeptide A levels (p = 0.002). Fibrinopeptide A levels correlated significantly (p < 0.001) with the presence of a filling defect (grade 4 intracoronary thrombus) or contrast staining (grade 3). All patients with fibrinopeptide A > or = 8 ng/mg creatinine showed grade 3 to 4 thrombus and 15 of 16 patients with levels > or = 6.0 ng/mg creatinine exhibited angiographic evidence of thrombus (13 with grades 3 to 4). Patients with reversible ST changes on the ECG had significantly higher levels of fibrinopeptide A (p < 0.001), and ST changes correlated significantly with the presence of angiographic thrombus (p < 0.001). Nonetheless, a significant minority of patients with unstable angina had neither angiographic nor biochemical evidence of thrombus., Conclusions: Elevated fibrinopeptide A levels in unstable angina reflected active intracoronary thrombus formation and were present in patients with angina of new onset as well as crescendo angina. Reversible ST changes are accompanied by thrombin activity and angiographic thrombus formation. However, a sizable percentage of patients with unstable angina had no evidence of thrombus and these patients may have had transient platelet aggregation without fibrin thrombus formation.

Patients with ostial left main coronary artery stenosis are at increased risk from diagnostic cardiac catheterization. In order to reduce this risk a modified Judkins coronary catheter with a sidehole 1.5-2 cm from the tip has been used in 6 patients in whom pressure damping was observed after initial use of a standard end-hole Judkins left coronary catheter. This eliminates damping and allows forceful hand injection with good proximal and distal vessel opacification. It also allows the acquisition of multiple views without the need for catheter removal after each injection, thereby reducing the risk involved in multiple cannulations of a vessel with a potentially unstable lesion at its origin. The technique has also been used for ostial lesions in a right coronary artery and a vein graft.

Hemodynamic and echocardiographic data from 33 consecutive patients undergoing cardiac transplantation were correlated with endomyocardial biopsy results to determine whether reversible restrictive hemodynamics accompany histologic evidence of transplant rejection. During the study period 251 biopsy specimens were obtained during periods of no histologic evidence of transplant rejection and 52 episodes of mild, 20 episodes of moderate, and one episode of severe rejection. Right atrial mean pressure increased significantly during episodes of moderate transplant rejection (9.9 +/- 6.2 mm Hg, p less than 0.001) compared with pressures obtained during periods when there was no evidence of rejection (4.6 +/- 3.2 mm Hg), mild rejection (5.8 +/- 3.9 mm Hg), or resolving rejection (4.3 +/- 3.4 mm Hg). Y descent was elevated during moderate rejection (9.6 +/- 4.2 mm Hg, p less than 0.001) compared with pressures during episodes of no rejection (5.6 +/- 2.5 mm Hg), mild rejection (6.6 +/- 2.7 mm Hg), and resolving rejection (5.8 +/- 3.1 mm Hg) and showed a wave morphology consistent with a restrictive hemodynamic pattern. Pulmonary capillary wedge pressure was increased during moderate rejection (14.4 +/- 6.4 mm Hg) when compared with pressures obtained during episodes of no rejection (10.2 +/- 5.8 mm Hg) or resolving rejection (10.2 +/- 5.4 mm Hg) (p less than 0.02). Sensitivity for a right atrial mean pressure of 11 mm Hg indicating moderate rejection was 41% with a specificity of 96%. Sensitivity for Y descent (greater than or equal to 10 mm Hg) was 52% and specificity was 94%.(ABSTRACT TRUNCATED AT 250 WORDS)

We report the safety and feasibility of the first three patients using cardiopulmonary bypass support at the Indiana University Medical Center during PTCA. All patients had severe left ventricular dysfunction. Cannulation was performed using 18- or 20-French cannulae of the femoral vessels, either surgically or percutaneously. After heparinization with an activated clotting time of greater than 450 seconds, cardiopulmonary bypass was instituted using the Bard CPS system. Flows ranged from 3.0 to 4.3 L/min. Normasol was used to prime the pump. Blood was retransfused back into the patient at the end of the procedure. Bleeding was a problem in case 1 at the arterial cannulation site and subsequently was corrected for cases 2 and 3. Coronary angioplasties were deemed technically successful. We conclude that high-risk angioplasty can be performed in patients with poor left ventricular function using cardiopulmonary bypass support in the cardiac catheterization laboratory. Further study is indicated.

Two cases are described of intraluminal coronary artery filling defects resembling thrombus caused by nonopacified collateral blood flow mixing with injected contrast just distal to a severe coronary artery stenosis. The term pseudothrombus is ascribed to this appearance to emphasize this differential diagnosis of intraluminal filling defects.

Regional left ventricular wall motion abnormalities were assessed using 2-dimensional echocardiography and contrast ventriculography within 12 hours of the onset of chest pain in 20 patients with acute myocardial infarction (AMI); 10 patients had anterior infarctions and 10 had inferior. End-diastolic and end-systolic sinus beats from right anterior oblique contrast ventriculograms were analyzed using the center-line chord technique with both a standard overlap method of chord assignment and a nonoverlap method. Echocardiograms were obtained in parasternal long- and short-axis and apical 2- and 4-chamber views and analyzed using a 16-segment scoring system to derive anterior and infero-posterolateral wall motion indexes using both overlap (10 segments for anterior, 8 inferior) as well as nonoverlap (9 segments anterior, 7 inferior) methods of segment assignment. There was a significant inverse correlation between the standard (nonoverlap) echocardiographic analysis and the standard (overlap) angiographic analysis for infarct regions (y = -0.43 X +1.11, r = -0.59, p less than 0.05). Fifteen of 18 patients with angiographic infarct regional score less than or equal to -1 standard deviation/chord had an echocardiographic index greater than or equal to 1.5, while 15 of 16 patients with echocardiographic regional infarct index greater than or equal to 1.5 had an angiographic score less than or equal to -1 standard deviation/chord. Correlation between the 2 methods for noninfarct territories was poor (r = -0.34) because the angiographic method assesses hyperkinesis while the echocardiographic method does not.(ABSTRACT TRUNCATED AT 250 WORDS)

Exercise echocardiography was performed in 36 patients to evaluate functional improvement after coronary angioplasty. Thirty-one patients (86%) had provokable ischemia before angioplasty including 22 with an abnormal exercise electrocardiographic test (angina or ST depression), 25 with an abnormal exercise echocardiogram (exercise-induced wall motion abnormalities) and 16 with both tests abnormal. Nineteen patients had no induced ischemia after angioplasty. Seventeen (47%) continued to have ischemia that was limited in 12 to exercise-induced wall motion abnormalities, which were less severe compared with those of preangioplasty studies. Fifteen (65%) of 23 patients had improvement in rest wall motion abnormalities after angioplasty. The rest to immediate postexercise change in global wall motion score was significantly improved after angioplasty. The change in regional wall motion score was significantly improved after angioplasty in patients with single vessel right or left circumflex coronary artery disease and approached significant improvement (p = 0.06) in those with single vessel disease of the left anterior descending coronary artery. Exercise echocardiography improves the sensitivity of functional testing for ischemia, aids in localizing the ischemic zone and documents improvement in regional function after coronary angioplasty.

To determine the role of tissue-type plasminogen activator (t-PA) and immediate percutaneous transluminal coronary angioplasty (PTCA) in treating patients with evolving transmural myocardial infarction, 50 patients received t-PA (1.25 mg/kg iv over 3 hrs) or placebo according to 3:1 double-blind randomization 3.8 +/- 1.1 hr after onset of symptoms. At emergency coronary arteriography, patency of the infarct-related vessel was demonstrated in 32 of 38 (84%) patients receiving t-PA vs two of 12 (17%) receiving placebo (p less than .001). Of the 32 patients with recanalization after t-PA, 28 had a residual stenosis of at least 50% and underwent randomization a second time to immediate (n = 15) or no PTCA (n = 13). Immediate PTCA of the infarct-related vessel was successful in all 15 patients, with reduction of the residual diameter stenosis from 80.8 +/- 8.2% to 32.5 +/- 15.6% (p less than .001). The incidence of postinfarction angina (greater than or equal to 20 min of chest discomfort and reversible electrocardiographic changes) and reinfarction (documented by recurrent creatine kinase isoenzyme elevation) was reduced in the patients receiving t-PA and PTCA (2/15) compared with that in patients receiving t-PA alone (7/13; p = .006). At 1 week there was no difference in patency of the infarct-related vessel (12/15 t-PA and PTCA vs 9/13 t-PA only) or in global ventricular functional change between the two groups (0.5 +/- 10.4 SD/chord for t-PA and PTCA vs -2.1 +/- 8.2 SD/chord for t-PA only).(ABSTRACT TRUNCATED AT 250 WORDS)

Although global and regional left ventricular (LV) function has been demonstrated to improve after reperfusion in acute myocardial infarction (AMI), the timing of these changes has not been well established. In this study, serial 2-dimensional echocardiography was used to assess regional LV function in 23 patients with AMI in whom reperfusion was accomplished by thrombolysis alone, by coronary angioplasty alone or by both interventions within 6 hours after onset of chest pain. Echocardiograms were performed before or within 6 hours after reperfusion (n = 23) and at 1 (n = 19), 3 (n = 21) and 7 (n = 20) days after reperfusion. Wall motion index and percentage of normally functioning muscle were calculated using a 16-segment scoring system analyzed in blinded fashion without knowledge of patient identity, therapy or time of study. The mean wall motion index improved from 1.78 +/- 0.48 to 1.56 +/- 0.38 at 1 day (n = 19, p less than 0.01), and to 1.48 +/- 0.37 at 3-7 days (p less than 0.01), with no significant difference between 3 days (1.49 +/- 0.39) and 7 days (1.42 +/- 0.30). There was a corresponding improvement in the percentage of normally functioning muscle, from 53 +/- 24% at 6 hours to 62 +/- 20% at 1 day (p less than 0.05) and to 67 +/- 18% at 3-7 days (p less than 0.01), again with no significant difference between 3 days (67 +/- 21) and 7 days (70 +/- 20).(ABSTRACT TRUNCATED AT 250 WORDS)

The haemodynamic effects of oral and intravenous salbutamol were investigated in 22 patients with chronic heart failure. Intravenous salbutamol (13 micrograms/min) increased cardiac index by 53 per cent from 1.5 +/- 0.13 1/min per m2 to 2.3 +/- 0.23 1/min per m2 and decreased systemic vascular resistance by 28 per cent from 29.4 +/- 3.9 units to 21.2 +/- 2.5 units. Heart rate rose by 10 per cent from 101 +/- 3.5 beats per minute to 111 +/- 3.2 beats per minute and pulmonary artery end-diastolic pressure fell by 13 per cent from 26.3 +/- 1.8 mmHg to 22.8 +/- 2.1 mmHg. Similar results were obtained after oral salbutamol (8 mg). Cardiac index rose by 40 per cent and systemic vascular resistance fell by 30 per cent. There was a small rise in heart rate and a variable and not significant change in pulmonary artery end-diastolic pressure. Experiments on isolated rabbit papillary muscle showed that salbutamol, at the concentration which exists in patients, had no detectable positive inotropic effect. It is probable that the increase in cardiac output in patients is primarily the result of reduced afterload caused by vasodilatation. Salbutamol is a useful drug in the treatment of chronic heart failure.

Acute increases in left ventricular (LV) diastolic pressure relative to volume occur during angina in humans and after pacing tachycardia in dogs with coronary stenoses. In this study we assessed myocardial function following pacing tachycardia in dogs with coronary stenoses and compared it with function of the same myocardial segment during coronary occlusion. Also we calculated regional wall stiffness following pacing tachycardia in dogs with coronary stenoses. In anesthetized dogs with two-vessel critical (90%) coronary stenoses, ultrasonic crystals were implanted subendocardially to measure either anterior wall (AW) and lateral wall (LW) segment lengths (SL; n = 14) or LV wall thickness (h; n = 7). LV pressure was measured using a high-fidelity micromanometer catheter. After pacing tachycardia in dogs with two-vessel coronary stenoses, there was a substantial rise in LV end-diastolic pressure (from 6 +/- 1 to 15 +/- 1 mmHg; P less than 0.001), a slight increase in end-diastolic segment length (AWEDSL from 15.6 +/- 1.0 to 16.4 +/- 1.0 mm; p less than 0.01; and LWEDSL from 13.8 +/- 1.4 to 14.3 +/- 1.4 mm; P greater than 0.01) and a reduction of percent systolic shortening of the ischemic segments. An upward shift of the diastolic pressure-SL relation was observed in the postpacing period. During coronary occlusion the diastolic pressure-SL relation of the same segment shifted rightward, or rightward and downward, and systolic shortening became holosystolic bulging. Ischemia due to coronary stenoses plus increased O2 demand had substantially different effects on regional wall motion and segmental diastolic mechanics than did ischemia due to coronary occlusion. Over the same range of residual transmural LV diastolic pressure, the radial stiffness modulus was higher after pacing tachycardia in the presence of coronary stenoses.

The hemodynamic effects of the cardioselective beta adrenergic blocking agent metoprolol, at a dose of 0.1 mg/kg body weight administered intravenously, were studied in 10 patients undergoing routine cardiac catheterization. The beta adrenergic blocking effect of the drug was confirmed by a highly significant reduction (53 percent, P less than 0.001) in the mean heart rate response to a challenge with isoproterenol, and by a mean heart rate rssponse to a challenge with isoproterenol, and by a highly significant reduction (73 percent, P less than 0.001) in the isoproterenol-induced increase in the first derivative of left ventricular pressure (dP/dt). An intrinsic negative inotropic effect was shown by a 43 percent reduction (P less than 0.05) in the response of mean left ventricular dP/dt when the heart rate was fixed by atrial pacing alone. With the combination of atrial pacing and isoproterenol, metoprolol produced a 48 percent reduction (P less than 0.01) in the response of mean left ventricular dP/dt, resulting from both the intrinsic depressor effect and the beta adrenergic blocking effect on the rate-independent beta agonist activity of isoproterenol. There was no significant change in right atrial, femoral arterial or left ventricular end-diastolic pressure; analysis of left ventricular angiograms performed during atrial pacing before and after metoprolol revealed no significant effect on angiographic ejection fraction, pressure-volume loops or diastolic compliance. In two patients improvement in segmental wall motion was noted, and no deterioration was seen in any patient. Metoprolol is an effective cardioselective beta adrenergic blocking agent that, under these conditions, reduces catecholamine-induced increases in heart rate and left ventricular dP/dt without significant alteration in ejection fraction, preload or afterload.

The effects on cardiac hemodynamics and serum parameters of a standard contrast agent (sodium methylglucamine diatrizoate [Renografin 76]) were compared with the effects of a new nonionic agent (iohexol) in a double-blind study in 51 patients undergoing coronary angiography and left ventriculography. No significant alteration in measured blood parameters occurred with either contrast agent. Hemodynamic changes occurred with both, but were significantly greater with the standard Renografin than with the low-osmolality, nonionic iohexol. After left ventriculography, heart rate increased and peripheral arterial pressure fell with both agents, but less with iohexol. Following coronary artery injections, heart rate and arterial pressure decreased with both agents, but the changes were more marked and occurred earlier with the standard contrast material. It is concluded that iohexol causes less alteration in cardiac function than does the agent currently most widely used. Nonionic contrast material is likely to improve the safety of coronary angiography, particularly in those patients at greatest risk.

The two-dimensional echocardiographic features of anomalies of systemic and coronary venous return are described as they were seen in 23 patients with this diagnosis proven at angiography. A left-sided superior vena cava draining to the right atrium via an enlarged coronary sinus was correctly identified in all 17 patients with this condition by observing a characteristically moving ovoid structure in the region of the posterior atrioventricular groove. This structure opacified before the right side of the heart following bolus injections of contrast material from a left arm vein. Injection from the right arm in 12 patients or femoral vein in four patients of this group produced contrast echoes within the right heart only. A left-sided superior vena cava draining directly to a left atrium in three patients, or left side of a common atrium in two patients with atrial situs inversus, was identified by the immediate opacification of the left-sided chamber following injection from the left arm. Two patients with hemiazygos inferior vena caval return to the left superior vena cava or left atrium were studied using injections of contrast from the femoral vein which successfully identified the venous abnormality. Two-dimensional echocardiography, when combined with peripheral venous injections of contrast will reliably demonstrate anomalies of systemic venous return, and thus provides important information before more invasive procedures.

The accumulation of calcium during myocardial hypoxia or ischaemia followed by reoxygenation or reperfusion is related to the development of cell necrosis and may be an important causal mechanism. Influx of calcium is a late event during hypoxia but occurs abruptly on reoxygenation or reperfusion. On reoxygenation calcium influx is not altered by nifedipine or quiescence but can be prevented by nickel (3 mM), cyanide (5 mM) or FCCP (10(-6) M). The extracellular marker 51Cr-EDTA does not enter the intracellular fluid on reoxygenation but can when the cell membrane is disrupted by a detergent, Brij'35, or the calcium paradox. The results suggest that the uptake of calcium on reoxygenation or reperfusion is related to the reintroduction of oxygen and caused by an increased calcium influx down the concentration gradient. The flux is not through the slow calcium channel and is not due to disruption of the membrane. The effects of CN- and FCCP and the unaltered calcium efflux suggest that the major part of the calcium uptake is stored in intracellular compartments and is not located in the intracellular fluid.

To compare the efficacy of emergency percutaneous transluminal coronary angioplasty and intracoronary streptokinase in preventing exercise-induced periinfarct ischemia, 28 patients presenting within 12 hours of the onset of symptoms of acute myocardial infarction were prospectively randomized. Of these, 14 patients were treated with emergency angioplasty and 14 patients received intracoronary streptokinase. Recatheterization and submaximal exercise thallium-201 single photon emission computed tomography were performed before hospital discharge. Periinfarct ischemia was defined as a reversible thallium defect adjacent to a fixed defect assessed qualitatively. Successful reperfusion was achieved in 86% of patients treated with emergency angioplasty and 86% of patients treated with intracoronary streptokinase (p = NS). Residual stenosis of the infarct-related coronary artery shown at predischarge angiography was 43.8 +/- 31.4% for the angioplasty group and 75.0 +/- 15.6% for the streptokinase group (p less than 0.05). Of the angioplasty group, 9% developed exercise-induced periinfarct ischemia compared with 60% of the streptokinase group (p less than 0.05). Thus, patients with acute myocardial infarction treated with emergency angioplasty had significantly less severe residual coronary stenosis and exercise-induced periinfarct ischemia than did those treated with intracoronary streptokinase. These results suggest further application of coronary angioplasty in the management of acute myocardial infarction.

A regional wall motion index has been derived from two-dimensional echocardiograms by use of a 16-segment model that was subdivided into anterior (nine segments) and infero-postero-lateral (seven segments) regions. This new method is compared with the use of a previously described global wall motion index for the analysis of serial echocardiograms after reperfusion in 23 patients who had acute myocardial infarction. Mean global index improved from 1.84 +/- 0.46 to 1.56 +/- 0.37 at 24 hours (p less than 0.01) and to 1.50 +/- 0.29 after 3 days to 7 days (p less than 0.02), whereas mean regional index for infarct regions improved from 2.28 +/- 0.73 to 1.82 +/- 0.58 at 24 hours (p less than 0.01) and to 1.70 +/- 0.42 after 3 to 7 days (p less than 0.01), with no significant change in the noninfarct index (1.34 +/- 0.32 initially and 1.28 +/- 0.36 after 3 to 7 days). Although both global and regional indexes effectively demonstrate early recovery of left ventricular function, (within 24 hours in many patients), the regional index for infarct regions is higher than the global index and effectively distinguishes between infarct and noninfarct segments. An overlap index in which an additional apical segment is included in the anterior region (10 segments) for anterior infarctions and in the infero-postero-lateral region (eight segments) for inferior infarctions results in a greater differentiation between infarct and noninfarct regions, with the mean initial noninfarct overlap index (1.17 +/- 0.33) significantly less than the nonoverlap index.(ABSTRACT TRUNCATED AT 250 WORDS)

A girl who presented in childhood with advanced primary pulmonary hypertension and whose condition later improved is described. This is the first time to our knowledge that documented regression of the disease has been reported.

An increase in left ventricular diastolic pressure has been repeatedly observed during angina in patients with coronary artery stenoses and regional demand ischemia, but the role of relaxation abnormalities versus left ventricular segmental dyssynchrony is controversial. In contrast, patients with angina due to aortic stenosis are likely to have diffuse rather than segmental ischemia and thus may provide an alternative model for examining the diastolic physiology of angina in man. Accordingly, we examined the hemodynamic manifestations of angina in eight patients with aortic stenosis without significant coronary artery disease. Angina was induced by pacing tachycardia, and hemodynamic and echocardiographic variables were measured in the control period and during angina in the beats immediately after cessation of pacing. Heart rate (control vs angina, 69 +/- 12 vs 70 +/- 11 beats/min, p = NS) and left ventricular peak systolic pressure (207 +/- 39 vs 222 +/- 22 mm Hg, p = NS) were similar in the control and postpacing angina periods. Left ventricular end-diastolic pressure, on the other hand, was significantly higher during postpacing angina (15 +/- 7 vs 28 +/- 8 mm Hg, p less than .01). The time constant of left ventricular pressure decline during isovolumetric relaxation (TL), calculated as the slope of a linear fit of the natural log of pressure vs time, increased from 44 +/- 5 to 51 +/- 7 msec (p less than .05); the time constant TD, derived from the slope of a linear fit of dP/dt vs pressure, also increased slightly, although the change was not statistically significant (69 +/- 5 vs 75 +/- 5 msec, p = .06).(ABSTRACT TRUNCATED AT 250 WORDS)

Quantitative global and regional ventriculographic analysis was performed acutely and 1 week later in 46 patients undergoing reperfusion procedures within 6 hours of acute inferior myocardial infarction due to right coronary artery disease. While serial improvement in global left ventricular ejection fraction was not demonstrated for the group, infarct zone regional wall motion did improve (-2.7 +/- 0.9 vs -2.3 +/- 1.4 SD/chord, p less than 0.007). Serial improvement in global ejection fraction was demonstrated in the subgroup of patients treated within 2 hours of symptom onset (55 +/- 10 vs 62 +/- 10%; n = 5; p less than 0.03). Infarct zone regional wall motion improved serially only in the subgroup of patients treated within 3 hours of symptom onset (-2.4 +/- 1.1 vs -1.3 +/- 1.7 SD/chord; n = 11; p less than 0.007). Patients with initially patent arteries had a higher ejection fraction on follow-up catheterization than did those with initially occluded vessels (61 +/- 11 vs 55 +/- 7%; p less than 0.02), and patients with patent arteries at follow-up had a higher ejection fraction than did those whose arteries were occluded (60 +/- 9 vs 48 +/- 4%; p less than 0.0001). We conclude that significant improvement in global and regional left ventricular function in patients with inferior myocardial infarction is possible when reperfusion therapy is begun early or when arterial patency is achieved.

The hemodynamic effects of CI-914, a phosphodiesterase inhibitor, were studied in 12 patients with left ventricular (LV) dysfunction who were undergoing diagnostic cardiac catheterization. CI-914 was infused intravenously at a rate of 0.8 to 7.0 micrograms/kg/min for 30 to 60 minutes; hemodynamic values were measured every 10 minutes. No effect was seen in the patient receiving 0.8 microgram/kg/min. At infusion rates of 1.2 to 2.4 micrograms/kg/min, cardiac index increased by 14% (p less than 0.025). At infusion rates of 4.5 to 7.0 micrograms/kg/min, cardiac index increased by 21% (n = 8, difference not significant [NS]). Among 4 patients (group B) with an initial pulmonary artery wedge pressure greater than 20 mm Hg and cardiac index less than 2.5 liters/min/m2, cardiac index increased by 50% (p less than 0.001); it did not change among the 4 patients with an initial pulmonary artery wedge pressure of less than 20 mm Hg and cardiac index of more than 2.5 liters/min/m2 (group A). Although systemic vascular resistance decreased in all 8 patients by 26% (p less than 0.01), the reduction was greater in group B (33%, p less than 0.01) than in group A (16%, NS). Peak +dP/dt increased in all 8 patients by 13% (p less than 0.01). Mean stroke work index increased from 29 +/- 15 to 34 +/- 13 g-m/m2; the double product fell from 101 +/- 31 to 91 +/- 23 (NS). In all 12 patients, a linear correlation between peak venous blood concentration and peak effect on cardiac index, systemic vascular resistance and pulmonary artery wedge pressure was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

A 59-year-old woman with a left atrial myxoma was shown to have moderate aortic regurgitation. At operation for removal of the myxoma it was found to be attached to the atrial septum close to the aortic root. It is suggested that the aortic regurgitation was caused by distortion of the aortic root caused by traction upon it from the myxoma as it moved downward into the left ventricle in diastole. Observations are made on the echocardiographic findings which helped in the diagnosis of the left atrial myxoma.

A 65-yr-old woman presented with severe congestive cardiac failure and physical signs of an atrial septal defect. Investigation by cardiac catheterisation and cross-sectional echocardiography showed a persistent left superior vena cava draining through an enlarged coronary sinus into the right atrium. In addition, the left atrium was connected to the coronary sinus by two defects in its lateral wall. The atrial septum was intact. The physiological result of this rare anatomical abnormality was a large left-to-right shunt with a small right-to-left component. The defects were closed surgically.

We randomly assigned 56 patients who presented within 12 hours of their first symptoms of acute myocardial infarction to treatment with either intracoronary streptokinase or coronary angioplasty. The mean (+/- SD) duration of symptoms (3.0 +/- 1.2 hours in the group treated with angioplasty vs. 3.6 +/- 1.8 in the group treated with streptokinase; P not significant) and time to recanalization (4.1 +/- 1.4 hours vs. 4.8 +/- 1.7 hours; P not significant) were similar in both groups. Coronary recanalization was achieved in 83 percent of the patients treated with angioplasty and in 85 percent of those treated with streptokinase (P not significant). Residual luminal stenosis in the coronary artery was significantly decreased after angioplasty, as compared with streptokinase therapy (43 +/- 31 percent of patients vs. 83 +/- 17; P less than 0.001). Residual stenosis of 70 percent or more was present in 4 percent of the angioplasty-treated patients and in 83 percent of the streptokinase-treated patients (P less than 0.01). Ventricular function after therapy was assessed by serial contrast ventriculograms. Increases in both global ejection fraction (8 +/- 7 percent vs. 1 +/- 6; P less than 0.001) and regional wall motion (+1.32 +/- 1.32 SD vs. +0.59 +/- 0.79 SD; P less than 0.05) were greater for the angioplasty group. We conclude that angioplasty and streptokinase produce similar rates of early coronary reperfusion during evolving transmural myocardial infarction. However, angioplasty is significantly more effective in alleviating the underlying coronary stenoses, and this may result in more effective preservation of ventricular function after therapy.

The hemodynamic effects of a new parenteral formulation of nifedipine administered by the intravenous (1 mg) and intracoronary (IC) (0.1 and 0.2 mg) routes were studied in 10 patients with symptomatic coronary artery disease undergoing diagnostic right- and left-sided cardiac catheterization. Intravenous nifedipine (1 mg) reduced systemic vascular resistance by 34% (p less than 0.01), increased cardiac output by 28% (p less than 0.01) and decreased mean arterial pressure by 10% (p less than 0.01). It had less effect on peak positive dP/dt (-8% p less than 0.025) and on peak negative dP/dt (-15% p less than 0.01). Coronary blood flow increased 20% (p less than 0.025). In contrast, IC nifedipine (0.2 mg) increased coronary blood flow 46% (p less than 0.025), depressed contractility as assessed by peak positive dP/dt (-26% p less than 0.01) and prolonged diastolic relaxation time. The effect of 0.1 mg was similar but less pronounced. These data suggest that the primary therapeutic effect of nifedipine administered systemically to patients at rest results from an increase in coronary blood flow and, to a lesser extent, from afterload reduction; its myocardial depressant effects are small, transient and masked by reflex catecholamine release. IC nifedipine increases coronary blood flow, has a transient negative inotropic effect and prolongs relaxation. The relative importance of these myocardial effects in preventing myocardial ischemia is not known.

This study quantitatively evaluated the change in myocardial blood flow resulting from medical revascularization in patients with acute anterior myocardial infarction. Changes in great cardiac vein flow were measured using a thermodilution technique in 13 patients with acute infarction; 3 received intracoronary streptokinase and 10 percutaneous transluminal angioplasty. Average great cardiac vein flow during left anterior descending coronary artery occlusion was 62 +/- 6 ml/min and increased to 70 +/- 7 ml/min (p = 0.039) after arterial recanalization. There was significant individual variability in the great cardiac vein flow increments that was highly predictive of functional recovery as expressed by the change in ejection fraction at 7 to 10 days (r = 0.93, p = 0.0008). Incremental great cardiac vein flow was inversely correlated with the degree of residual stenosis and the duration of ischemia (r = 0.88, p = 0.0007). Patients with residual stenosis less than or equal to 50% had a significantly larger increase in great cardiac vein flow (14 +/- 5 ml/min) than did those with residual stenosis greater than 50% (0 +/- 2 ml/min, p = 0.026). Neither preinterventional left ventricular ejection fraction, hemodynamics nor age predicted incremental great cardiac vein flow. Therefore, quantitative measurements of great cardiac vein flow during medical revascularization in patients with an acute anterior myocardial infarction demonstrate variable reflow that is physiologically significant. A high grade residual stenosis and prolonged period of ischemia limit large increases in flow and prevent functional recovery. This study emphasizes the fact that recanalization in itself cannot be used as an indicator of the success of interventions designed to produce myocardial reperfusion.

Cardiac output estimation by thermodilution is carried out using room temperature or iced injectate, but the accuracy and variability of the two methods is not well documented. Room temperature and iced injectate were compared in 21 patients undergoing diagnostic cardiac catheterization. Dextrose injectate (10 ml) was administered in prefilled syringes left to stand either in iced water or in room air. Four injections were made sequentially with room temperature and iced injectate. Cardiac output by room temperature and iced injectate were not significantly different (4.70 +/- 1.22 for room temperature and 4.90 +/- 1.37 for iced injectate, n = 21, P = 0.155). There was a significant difference in the variance of the estimations by the two methods (room temperature = 0.296, iced = 0.120, P less than 0.005). From this variance the calculated number of measurements needed to estimate cardiac output to +/- 0.5 L/min with 95% confidence is seven for room temperature and four for iced injectate. For five patients with cardiac output less than 4.00 L/min with room temperature injectate, cardiac output with iced injectate was significantly higher (3.33 +/- 0.34 for room temperature vs. 3.69 +/- 0.49 for iced injectate, P = 0.05). Thus room temperature injectate generally gives a satisfactory cardiac output estimation but with significantly greater variability than iced injectate. Sample size for accurate cardiac output estimation must be greater with room temperature injectate. Iced injectate may over-estimate output when cardiac output is low.

Eight months after triple valve replacement with Björk-Shiley tilting disc valves a patient developed symptoms and signs suggesting malfunction of the prosthesis in the tricuspid position. This was confirmed by echocardiography and angiocardiography, and at operation thedisc of the prosthesis was found to be stuck half-open by fibrin and clot. A further 11 patients with the same tupe of prosthesis in the triscupid position were then studied by phonocardiography and echocardiography. In one of these the prosthesis was found to be stuck and this was confirmed by angiocardiography and surgery. These 2 cases are reported in detail and the findings in the other 10 are discussed. The implications of this high incidence of malfunction of the Björk-Shiley prosthesis in the tricuspid position are considered. Echocardiography appears to be essential in the follow-up of such patients.

Transient myocardial depression associated with intracoronary injections of contrast medium has been attributed to hypertonicity and to calcium binding. To further assess the importance of calcium binding, a new technique for continuous monitoring of coronary sinus ionized calcium with an intravascular calcium-selective electrode was used. With this calcium-selective electrode the effects of intracoronary injection in dogs of a conventional ionic contrast agent, sodium meglumine diatrizoate (Renografin-76), and a new nonionic agent, iohexol, were assessed and compared. Left ventricular pressure was measured with a micromanometer catheter. After bolus injection of 0.2 ml/kg body weight of Renografin-76 (n = 10), coronary sinus pCa increased by 0.27 from 2.98 +/- 0.02 to 3.25 +/- 0.03, indicating a decrease in ionized calcium from 2.0 to 1.1 mEq/liter. With iohexol (n = 9), pCa increased by only 0.05 +/- 0.01 (p less than 0.001), indicating a decrease in ionized calcium from 2.0 to 1.8 mEq/liter. Peak changes occurred approximately 6 seconds after injection. Renografin-76 caused a marked decrease in left ventricular systolic pressure (140 +/- 7 to 106 +/- 8 mm Hg) and in heart rate (122 +/- 7 to 101 +/- 5 beats/min) with an increase in end-diastolic pressure (5 +/- 1 to 12 +/- 1 mm Hg), whereas iohexol did not significantly alter these variables. Using Renografin-76 with calcium added to achieve an ionized calcium level of 2 (n = 4), 4 (n = 4) or 6 (n = 4) mEq/liter, the changes in coronary sinus pCa were abolished and the hemodynamic changes attenuated. These findings indicate that Renografin-76 results in greater myocardial depression than the new nonionic agent iohexol.(ABSTRACT TRUNCATED AT 250 WORDS)

Fifty patients undergoing successful reperfusion therapy (percutaneous transluminal coronary angioplasty 20, thrombolysis 10, combined 20) for acute myocardial infarction were evaluated with serial two-dimensional echocardiograms performed early (less than 24 hours, mean 8 hours) and late (greater than 3 days, mean 6 days) after presentation. Treatment occurred within 12 hours of the onset of symptoms with most patients achieving reperfusion in less than 6 hours (mean 4.7 hours) from the onset of pain. Reperfusion was demonstrated short-term by angiography in 42 of 50 patients (84%). Four patients had clinical signs of reperfusion and subsequent angiographic confirmation. An additional four patients with "stuttering" infarct courses were treated late by percutaneous transluminal coronary angioplasty. Echocardiograms were analyzed for global performance by calculation of fractional area change at the papillary muscle level and ejection fraction (biplane Simpson's rule) in 18 patients in whom this analysis could be performed. Measurements of regional function included fractional shortening at the base (n = 37), regional wall motion index (n = 50) and percent of normal functioning myocardium (n = 50). Overall there was a significant improvement in regional wall scores and percent of functioning myocardium (regional wall motion index 1.73 to 1.43, p less than 0.001 and percent of functioning myocardium 0.61 to 0.70, p less than 0.001) but only a trend toward improvement when global function was assessed by ejection fraction (0.42 to 0.48, p less than 0.14).(ABSTRACT TRUNCATED AT 250 WORDS)

The upward shift in the left ventricular diastolic pressure-volume relationship during pacing-induced angina may be related to increased cytosolic calcium availability with persistent contractile element interaction in diastole. To assess the influence of calcium channel blockade on these changes in diastolic function, we studied the effects of verapamil in dogs with 90% stenoses of the left anterior descending and circumflex coronary arteries. Ultrasonic crystals were implanted in the myocardium to monitor anterior wall and lateral wall segment length. Left ventricular pressure was measured with a micromanometer catheter. The left atrium was paced at a rate 1.5 times that of the resting heart rate for 3 min. An upward shift of the left ventricular diastolic pressure-segment length relationship developed after pacing tachycardia, with a rise in the left ventricular end-diastolic pressure (LVEDP) from 4.7 +/- 1.2 to 14.3 +/- 2.2 mmHg (P less than 0.01, n = 13), and pressure was higher at any segment length throughout diastole. Increases in end-diastolic segment length were small (12.3 +/- 1.9 to 12.7 +/- 2.0 mm for the anterior wall, P less than 0.05; 15.1 +/- 1.4 to 16.4 +/- 1.5 mm for the lateral wall, P less than 0.01). Pretreatment with verapamil (0.08 mg/kg iv) did not reduce this upward shift: LVEDP rose from 6 +/- 1 to 16 +/- 1 mmHg (P less than 0.01, n = 7) and there were similar small increases in end-diastolic segment length.(ABSTRACT TRUNCATED AT 250 WORDS)

A method is described with which the extracellular space of isolated ventricular muscle can be measured accurately and continuously in the same muscle. The size of the extracellular space is shown to vary with the contractile state of the myocardium. Interventions such as quiescence, manganese and acidosis reduce myocardial contractility and increase the size of the extracellular space. Barium, ouabain and hypoxia cause contracture and reduce the size of the extracellular space. These changes should be taken into account when measuring intracellular electrolytes in isolated ventricular preparations.

We have studied calcium exchanges and mechanical function in heart muscle during and after a period of ischaemia. The experimental preparation was the isolated but arterially perfused interventricular septum of the rabbit. Uptake of calcium was measured with 47Ca2+ and efflux with 45Ca2+. 51Cr-EDTA was used as a marker of the extracellular space. Ischaemia caused a rapid decline of developed tension followed by a rise in resting tension. Tissue counts of 47Ca2+ decreased due to a reduction in the extracellular space. On reperfusion after ischaemia developed tension partially recovered and resting tension increased further before returning towards control values. A large and prolonged uptake of 47Ca2+ occurred immediately on reperfusion while 45Ca2+ efflux rose transiently. The uptake of calcium was related to the severity and duration of ischaemia and to the degree of mechanical recovery. Calcium accumulation on reperfusion is due to an increased influx which is not related to gross disruption of the cell membrane but more probably to a specific abnormality of ionic channels.