bluuebunny/crossref_metadata_2025 huggingface dataset:
Dilation angioplasty of congenital or operative narrowings of venous channels.
Authors: Lock J E , Bass J L , Castaneda-Zuniga W , Fuhrman B P , Rashkind W J , Lucas R V
Published: June 2011

Balloon dilation angioplasty was attempted in 10 infants and children with severe congenital or operative "venous" obstructions. In five children the obstructions were "vena caval" and followed repair for transposition of the great vessels (four patients) or orthotopic liver transplantation (one patient). In the four patients with fixed vena caval or baffle obstructions, balloon angioplasty was successful in relieving the obstruction, decreasing the average gradient (16.0 to 4.5 mm Hg), and increasing the average diameter (3.0 to 8.9 mm) of the obstructed site. One child died 1 week later from an unrelated cerebral hemorrhage; the three survivors have had persistent clinical and angiographic improvement. The fifth child had severe systolic narrowing of the superior baffle limb caused by marked tricuspid regurgitation, which ballooned the superior limb of the baffle against the atrial roof. Angioplasty was unsuccessful in relieving this type of obstruction, which resolved with tricuspid valve replacement. Of the five infants with obstructed pulmonary veins, three had congenitally narrowed vessels associated with total anomalous pulmonary venous connection, one had acquired stenosis, and one had postoperative obstruction after repair of a mixed type of total anomalous pulmonary venous connection. Dilation was unsuccessful in all five patients, but for different reasons: in the congenitally narrowed veins, the waist in the balloon could not be eliminated, even with high dilating pressures; in the infant with acquired stenosis, the vein stretched but did not tear at low dilating pressures; and in the postoperative obstruction, angioplasty increased the diameter of the obstruction but did not increase flow to the affected lung.(ABSTRACT TRUNCATED AT 250 WORDS)
Efficacy and safety of timolol for prevention of supraventricular tachyarrhythmias after coronary artery bypass surgery.
Authors: White H D , Antman E M , Glynn M A , Collins J J , Cohn L H , Shemin R J , Friedman P L
Published: June 2011

Forty-one patients undergoing coronary artery bypass grafting were randomly assigned to receive prophylactic timolol or placebo, given in a double-blind fashion. beta-Adrenoceptor-blocking therapy was stopped at least one half-life before surgery. Three to 7 hr after surgery (304 +/- 56 min), 0.5 mg of timolol or placebo was given intravenously twice daily in a double-blind manner. When oral medications were resumed postoperatively, 10 mg of timolol twice daily or placebo was continued orally. Continuous electrocardiograms were recorded for 24 hr before and for 7 days after surgery with a standard cassette recorder. No patient received digoxin. Both groups were comparable for frequency of preoperative supraventricular arrhythmias, left ventricular ejection fraction, duration of cardiopulmonary bypass, aortic cross-clamp time, number of bypass grafts, and total duration of monitoring. Analysis of arrhythmias was done by hand counts, and supraventricular arrhythmias were divided into supraventricular tachycardia and atrial fibrillation and/or flutter. Timolol decreased the frequency of supraventricular tachycardia (581 episodes placebo vs 84 timolol; p less than .05) and of atrial fibrillation and/or flutter (291 episodes placebo vs five timolol; p less than .05). Timolol decreased the number of patients with severe (heart rate greater than 200 beats/min, duration greater than 50 beats) episodes of supraventricular tachycardia (four placebo vs 0 timolol; p less than .05) and also decreased the number of episodes of severe (heart rate greater than 200 beats/min, duration greater than 5 min) atrial fibrillation and/or flutter (16 placebo vs one timolol; p less than .005). There were differences in the durations of supraventricular arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)
Long-term survival after prehospital cardiac arrest: analysis of outcome during an 8 year study.
Authors: Myerburg R J , Kessler K M , Estes D , Conde C A , Luceri R M , Zaman L , Kozlovskis P L , Castellanos A
Published: June 2011

We analyzed long-term follow-up data accumulated during an 8 year study of survivors of prehospital cardiac arrest. All patients included in this study were primary entrants via community-based rescue systems; patients who were tertiary referrals (survivors of cardiac arrest from other hospitals) were not included in this analysis. In the group of 61 patients entering our study between 1975 and 1980, with a follow-up to 1983, there have been a total of 24 deaths (39%). Sixteen of the 24 deaths were the result of recurrent cardiac arrest; eight were nonsudden cardiac deaths or noncardiac deaths. The mean duration from entry to death in the nonsurvivors was 27.5 +/- 19.7 months, and the time from the index event to last follow-up in the long-term survivors was 59.9 +/- 19.4 months. Life table analysis demonstrated a 10% rate of recurrence of cardiac arrest in the first year, with a 5% per year rate in each of the subsequent 3 years. Left ventricular ejection fractions at entry were not significantly different between survivors (mean = 45.3 +/- 13.6%) and nonsurvivors (mean = 37.6 +/- 12.6%), and the severity of ejection fraction abnormality at entry did not correlate with time to death in the nonsurvivors. However, ejection fraction was significantly lower in patients who died from causes other than recurrent cardiac arrest than in those who died of cardiac arrest (24.5 +/- 9.1% vs 42.7 +/- 9.2%; p less than .002).(ABSTRACT TRUNCATED AT 250 WORDS)
A randomized trial of intravenous and intracoronary streptokinase in patients with acute myocardial infarction.
Authors: Anderson J L , Marshall H W , Askins J C , Lutz J R , Sorensen S G , Menlove R L , Yanowitz F G , Hagan A D
Published: June 2011

The clinical effects of intravenous streptokinase in patients with acute myocardial infarction were compared with those of intracoronary streptokinase in a randomized, prospective study. Comparisons were also made with a historical control group. Fifty patients were entered into the study at 2.4 +/- 1.2 hr after onset of pain, and 27 were assigned to intravenous and 23 to intracoronary therapy. The doses of streptokinase averaged 212,000 U ic and 845,000 U iv (0.75 X 10(6) U/5 hr, n = 14 or 10(6) U/1 hr, n = 13). Results of studies of the two intravenous dosage schedules were similar and so were combined. Streptokinase was administered at 2.8 +/- 1.0 hr after onset of pain in the intravenous and at 4.3 +/- 1.4 hr in the intracoronary drug group (p less than .001). Convalescent (day 10) radionuclide ejection fractions were 54 +/- 14% for the intravenous and 50 +/- 16% for the intracoronary drug group. Change in ejection fraction from day 1 to 10 tended to be greater after intravenous drug: 5.1% (p less than .08) vs 1.2% (NS). Semiquantitative regional wall motion indexes in the infarct zone showed significant and similar modest improvement from admission to day 10 in both groups (p less than .02). Accelerated enzyme-release kinetics were noted after both therapies. Times of peak enzyme levels for patients on intravenous and intracoronary drug were, respectively, 12.5 +/- 5.0 and 11.5 +/- 4.3 hr for creatine kinase MB isoenzyme and 31.7 +/- 11.8 and 28.1 +/- 12.7 hr for lactic dehydrogenase (LDH). Peak LDH-1 level was lower in patients receiving intravenous drug than in the historical control group (p less than .05). Electrocardiographically summed ST segments diminished rapidly after therapy in both groups; Q wave development was similar and overall R wave loss was equivalent and less extensive compared with in historical control subjects. Infarct pain requiring morphine was diminished similarly in both treatment groups. Incidence of early arrhythmias and heart failure also did not differ. Posttherapy ischemic events and early surgery tended to be more common in the intracoronary group and bleeding was more common in the intravenous group. Intravenous drug did not decrease early hospital mortality (intravenous drug = 5, historical control = 4, intracoronary drug = 1); the differences in this parameter among groups were not significant. At convalescent angiographic evaluation, anterograde perfusion was present in 73% of those receiving intravenous and 76% of those receiving intracoronary drug.(ABSTRACT TRUNCATED AT 400 WORDS)
Increased risk of severe protamine reactions in NPH insulin-dependent diabetics undergoing cardiac catheterization.
Authors: Stewart W J , McSweeney S M , Kellett M A , Faxon D P , Ryan T J
Published: June 2011

Protamine is widely used for reversing systemic heparinization after cardiac catheterization. Although rare, major reactions to protamine that simulate anaphylaxis occasionally occur and have previously been associated only with an allergic reaction to fish. Because neutral protamine Hagedorn (NPH) insulin includes protamine, it might be anticipated that NPH insulin-dependent diabetic patients would develop sensitivity to protamine. Of 866 consecutive patients undergoing cardiac catheterization over a 20 month period, 651 received protamine for reversal of heparinization. Of these, 8.5% (56/651) were diabetics and 2.3% (15/651) were NPH insulin-dependent diabetics. During this period seven patients were observed immediately after administration of protamine to have major adverse reactions that required the administration of catecholamines. One death ensued. Of the seven major reactions, four occurred in NPH insulin-dependent diabetics and one occurred in a patient with an allergy to fish. The incidence of major protamine reactions was 27% (4/15) in the NPH insulin-dependent diabetics vs 0.5% (3/636) in those with no history of NPH insulin use (p less than .001). This represents a 50-fold increased risk of a major reaction to protamine if the patient was receiving NPH insulin. Accordingly, we recommend that diabetics on NPH insulin and patients with allergies to fish undergo cardiac catheterization without the use of protamine or, when necessary, that protamine be administered cautiously in anticipation of a major adverse reaction.
Comparison of enzymatic and anatomic estimates of myocardial infarct size in man.
Authors: Hackel D B , Reimer K A , Ideker R E , Mikat E M , Hartwell T D , Parker C B , Braunwald E B , Buja M , Gold H K , Jaffe A S
Published: June 2011

Enzymatic estimates of myocardial infarct size based on plasma levels of MB creatine kinase (MB-CK) were compared with anatomic infarct size in 49 human hearts obtained at autopsy. The patients studied had been enrolled in the Multicenter Investigation of Limitation of Infarct Size (MILIS) study program within 18 hr of the onset of acute infarction and were treated at one of five participating hospitals. Infarct size was estimated from serial measurements of plasma MB-CK made at the core laboratory for CK analysis. Hearts obtained at autopsy were studied independently by the core pathology laboratory without knowledge of the MB-CK levels or clinical results. Data from the two laboratories were compared at the data coordinating center. Of 49 hearts, 12 were excluded either because anatomic infarct size could not be established or because the infarct occurring at the time of enrollment in the MILIS study could not be distinguished with certainty from other infarcts. Of the remaining 37 hearts, peak MB-CK level was available in 36, but samples sufficient for estimation of infarct size were available in only 25. The overall correlation coefficient (Spearman) was .87 for these 25 hearts, indicating that enzymatic estimates of infarct size correlate closely with anatomic measurements. The results indicate that CK estimates of myocardial infarct size represent a valid clinical end point for assessing myocardial infarct size, and the effect of therapy thereon, in groups of treated and control patients.
Vasodilative effect of hydralazine in awake dogs: the roles of prostaglandins and the sympathetic nervous system.
Authors: Maekawa K , Liang C S , Tsui A , Chen B T , Kawashima S
Published: June 2011

The relative roles of prostaglandins and the sympathetic nervous system in mediating the hypotensive effects of hydralazine were studied in awake dogs with and without pretreatment with indomethacin, propranolol, and phentolamine. In normal dogs, mean aortic pressure decreased 23 +/- 4 mm Hg after administration of hydralazine (cumulative dose of 0.8 mg/kg). This hypotensive effect of hydralazine was potentiated by phentolamine but was abolished by propranolol. Indomethacin caused a paradoxic pressor response (11 +/- 3 mm Hg) to hydralazine, which also was abolished by addition of phentolamine. Hydralazine produced vasodilation in the coronary, skeletal muscle (quadriceps), splanchnic, and renal circulations in normal dogs. The increase in coronary blood flow was associated with increased cardiac oxygen consumption and narrowed arteriovenous oxygen difference across the heart. Propranolol reduced the increases in cardiac oxygen consumption and coronary blood flow, but only indomethacin abolished the narrowed arteriovenous oxygen difference, suggesting that the increase in coronary blood flow was related to both the increased cardiac oxygen demand and prostaglandin-mediated active coronary vasodilation. The decrease in skeletal muscle vascular resistance after hydralazine was abolished by propranolol. Skeletal muscle vascular resistance actually increased after administration of hydralazine in dogs pretreated with both propranolol and indomethacin. These effects were blocked by the addition of phentolamine. Unlike the normal response, renal and splanchnic vascular resistances increased after administration of hydralazine in dogs pretreated with indomethacin. The splanchnic vasoconstriction was abolished by phentolamine, but the renal vascular change was affected by neither phentolamine nor propranolol. The results indicate that hydralazine does not produce uniform vasodilation in all organs and that the cardiovascular actions of hydralazine involve both prostaglandins and the sympathetic nervous system.
Usefulness of the postexercise response of systolic blood pressure in the diagnosis of coronary artery disease.
Authors: Amon K W , Richards K L , Crawford M H
Published: June 2011

The normal decline in systolic blood pressure (SBP) during the recovery phase of treadmill exercise does not occur in some patients with coronary artery disease (CAD). In others the recovery values of SBP exceed the peak exercise values. To examine the diagnostic value of this observation, we studied 31 normal subjects and 56 patients undergoing treadmill exercise before coronary cineangiography. Because of large differences in peak exercise pressures between the two groups, recovery ratios were derived by dividing the SBP at 1, 2, and 3 min after exercise by the peak exercise SBP. The 1, 2, and 3 min ratios in the normal subjects declined steadily from 0.85 +/- 0.07 (SD) to 0.79 +/- 0.06 and to 0.73 +/- 0.06, respectively, while the ratios in the patients with CAD remained elevated at 0.97 +/- 0.12 to 0.97 +/- 0.11 to 0.93 +/- 0.13. With use of the upper limits defined by two SDs of the normal value, recovery ratios were compared with the occurrence of angina and with ST segment depression on the exercise electrocardiogram in the patients with CAD. Abnormal ratios were more frequent in patients with CAD (53/56, 95%) than in those with ST segment depression (33/56, 59%), angina (37/56, 66%), and either ST segment depression or angina (42/56, 75%). Twenty of the patients with CAD who were on no medication underwent an additional treadmill exercise test on a separate day and no significant differences were found in the ratios from the two tests. Ten additional patients with CAD underwent treadmill exercise testing while on placebo and while on a beta-blocker.(ABSTRACT TRUNCATED AT 250 WORDS)
Sustained improvement of pulmonary hemodynamics in patients at rest and during exercise after thrombolytic treatment of massive pulmonary embolism.
Authors: Schwarz F , Stehr H , Zimmermann R , Manthey J , Kübler W
Published: June 2011

This study assessed the long-term effects of thrombolytic treatment in patients with acute massive pulmonary embolism (PE). Seven patients with PE that followed deep-vein thrombosis underwent pulmonary angiography and pressure measurements before and 6 +/- 3 days (mean +/- SD) and 15 +/- 4 months after treatment with intrapulmonary infusions of urokinase (average dose 1724 U/kg X hr) and heparin (average dose 17 U/kg X hr). Treatment was guided by daily measurements of pulmonary arterial (PA) pressure and was continued until PA pressure had normalized (average of 6 days). Late after treatment patients returned for pulmonary angiographic examination, right heart catheterization at rest and during bicycle exercise, and phlebography of the deep veins of both legs. Pulmonary angiograms showed massive obstruction before therapy (Walsh index 15 +/- 2 points of a maximum of 18 points), which was improved 6 days (3 +/- 3 points) and 15 months (1 +/- 2 points) after therapy. Mean PA pressure declined from 37 +/- 9 to 13 +/- 3 mm Hg after 6 days and to 15 +/- 3 mm Hg after 15 months. No recurrence of PE was observed. In six of seven patients at rest and during bicycle exercise (up to 100 W) in the supine position mean PA pressure and total pulmonary resistance remained within normal limits. Over the short term all patients showed clinical signs of deep-vein thrombosis; 15 months later four patients had normal deep veins, but three patients had still phlebographic signs of old thrombosis.(ABSTRACT TRUNCATED AT 250 WORDS)
Spontaneous mitral valve prolapse in a breeding colony of rhesus monkeys.
Authors: Swindle M M , Blum J R , Lima S D , Weiss J L
Published: June 2011

Mitral valve prolapse was observed in 26 of 92 animals in a harem breeding colony of rhesus monkeys (Macaca mulatta). The affected animals had a systolic murmur best auscultated over the mitral region with the animal in a sitting position. Mid-to-late systolic clicks were also heard. Phonocardiographic examination also demonstrated systolic murmurs and clicks in six of 16 animals. Twenty-three of the animals were studied by M mode and/or two-dimensional echocardiography. The diagnosis was confirmed in 12 animals that had a murmur during the examination. Electrocardiograms revealed T wave abnormalities in five animals and left or right ventricular hypertrophy in five. Four adult animals that died during the course of the study were confirmed at necropsy as having prolapse of the posterior and/or anterior mitral valve leaflets into the atrium. Analysis of the breeding records suggested that mitral valve prolapse was a dominant genetic trait with an approximate birth incidence of 16% to 20% in the colony. The existence of mitral valve prolapse in a nonhuman primate species provides a unique opportunity to study the disease in an experimental animal.
Low-level exercise testing after myocardial infarction: usefulness in enhancing clinical risk stratification.
Authors: Krone R J , Gillespie J A , Weld F M , Miller J P , Moss A J
Published: June 2011

Of 866 patients enrolled in our multicenter study, 667 performed a low-level exercise test early after myocardial infarction, most before discharge. Excluding seven patients who died before the test could be considered, there was a 14% 1 year cardiac mortality in 192 patients who did not take the test (150 for medical and 42 for logistic reasons) compared with 5% in those who did (p less than .0001). Of those who took the test, 12% subsequently underwent bypass grafts surgery compared with 14% of those who did not (p greater than .05). Decreased mortality in the year after the infarction in those taking the test was associated with an increase in blood pressure to 110 mm Hg or higher (3% vs 18%; p less than .001), ability to complete the 9 min test (3% vs 8%; p less than .01), and the absence of couplets (4% vs 13%; p less than .05) or any ventricular ectopic depolarizations (4% vs 7%, p less than .05) before, during, or after exercise. Achievement of a blood pressure of 110 mm Hg or higher during exercise in patients with no evidence of pulmonary congestion on the chest x-ray identified a group of 454 patients (70% of those taking the test) with a 1 year cardiac mortality of 1% compared with 13% in the remaining patients (p less than .0001). Logistic models showed that the exercise test contributed independent prognostic information for cardiac death, new infarction, and bypass surgery. Results of low-level exercise testing before hospital discharge combined with clinical features of the infarction can effectively identify patients at low risk for subsequent cardiac mortality.
Prognosis after extension of myocardial infarct: the role of Q wave or non-Q wave infarction.
Authors: Maisel A S , Ahnve S , Gilpin E , Henning H , Goldberger A L , Collins D , LeWinter M , Ross J
Published: June 2011

We examined whether or not subsets of patients with extension of myocardial infarct were at high risk for early and late mortality. Some data suggest increased risk in patients with non-Q wave infarcts and we hypothesized that infarct extension in this group might be associated with a poorer prognosis than that for patients with extension of Q wave infarcts. A total of 1253 patients with acute myocardial infarction who were included in our data base were followed prospectively. The patients were classified according to electrocardiographic results into the following groups: those with non-Q wave (n = 277) infarcts and those with Q-anterior (n = 462) and Q-inferior (n = 497) infarcts. Extension was diagnosed by two of the following criteria: (1) recurrent chest pain 24 hr or more after admission to the hospital, (2) new persistent electrocardiographic changes, and (3) elevation or reappearance of creatine kinase. By these criteria 85 (6%) patients had extension (8% of non-Q wave infarcts, 6% of Q-anterior infarcts, and 6% of Q-inferior infarcts). Hospital mortality in patients with extension was 15% in those with Q wave infarcts vs 43% in those with non-Q wave infarcts (p less than .01). Nine hundred and fifty-two patients were followed for 1 year. In 24% of those who did not survive 1 year there was extension of infarct; only 6% of survivors had extension (p less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)
Left ventricular dysfunction in patients with angina pectoris, normal epicardial coronary arteries, and abnormal vasodilator reserve.
Authors: Cannon R O , Bonow R O , Bacharach S L , Green M V , Rosing D R , Leon M B , Watson R M , Epstein S E
Published: June 2011

Thirty-three patients with chest pain despite angiographically normal coronary arteries underwent both coronary flow studies during pacing and resting and exercise gated blood pool scintigraphy. During atrial pacing after administration of ergonovine, those patients developing their typical chest pain demonstrated significantly lower great cardiac vein flow (97 +/- 31 vs 150 +/- 33 ml/min, p less than .001), higher coronary resistance (1.27 +/- 0.43 vs 0.77 +/- 0.18 mm Hg/ml/min, p less than .005), and less lactate consumption (30.5 +/- 22.0 vs 69.7 +/- 41.1 mM . ml/min, p less than .005) and a higher left ventricular end-diastolic pressure after pacing (20 +/- 4 vs 12 +/- 1, p less than .001) compared with those without pain and in the absence of significant luminal narrowing of the epicardial coronary arteries. The 26 patients with abnormal vasodilator reserve demonstrated reduced left ventricular ejection fraction during exercise (58 +/- 8%) compared with the seven patients with appropriate vasodilator reserve (66 +/- 4%, p less than .05) and with a group of 52 control patients of similar age and sex distribution and free of known heart disease (66 +/- 10%, p less than .001). In addition, 12 of the 26 patients with abnormal vasodilator reserve demonstrated exercise-induced regional wall motion abnormalities. Many of these patients also manifested impaired left ventricular diastolic filling at rest compared with the control subjects (peak filling rate 2.6 +/- 0.7 vs 3.2 +/- 0.7 end-diastolic volume/sec, p less than .005). Thus, patients with chest pain resulting from abnormal vasodilator reserve demonstrate abnormalities of left ventricular systolic and diastolic function suggestive of myocardial ischemia.
Altered effect of the Valsalva maneuver on left ventricular volume in patients with cardiomyopathy.
Authors: Little W C , Barr W K , Crawford M H
Published: June 2011

The failure of the blood pressure to fall during the late strain pase of the Valsalva maneuver in patients with heart failure may result from the left ventricle operating on a flat portion of its function curve or from maintenance of left ventricular volume despite decreased systemic venous return. To test these possibilities, we studied the effect of the Valsalva maneuver (40 cm H2O for 15 sec) on left ventricular volume in 12 normal subjects with a mean left ventricular ejection fraction of 0.65 +/- 0.07 (+/- SD) and in eight patients with nonischemic cardiomyopathy, evidence of pulmonary congestion, and a mean left ventricular ejection fraction of 0.23 +/- 0.09. Left ventricular volume and right ventricular area were determined by apical two-dimensional echocardiography. In both groups the right ventricular end-diastolic area decreased during the late strain phase of the Valsalva maneuver. In normal subjects it decreased from 9.3 +/- 1.5 to 5.6 +/- 1.6 cm2 (p less than .001) and in patients it decreased from 13 +/- 2.2 to 10 +/- 2.9 cm2 (p less than .001). In normal subjects, left ventricular end-diastolic volume decreased from the control level during the Valsalva maneuver, and this was apparent in both the four-chamber (96 +/- 21 to 68 +/- 18 ml, p less than .01) and two-chamber views (97 +/- 15 to 56 +/- 20 ml, p less than .01). In the patients, left ventricular end-diastolic volume was not significantly different from control in either view (199 +/- 70 to 195 +/- 78 and 214 +/- 77 to 218 +/- 86 ml, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
Myocardial ischemia in patients with hypertrophic cardiomyopathy: contribution of inadequate vasodilator reserve and elevated left ventricular filling pressures.
Authors: Cannon R O , Rosing D R , Maron B J , Leon M B , Bonow R O , Watson R M , Epstein S E
Published: June 2011

To study the mechanism and hemodynamic significance of myocardial ischemia in hypertrophic cardiomyopathy, 20 patients (nine with resting left ventricular outflow tract obstruction greater than or equal to 30 mm Hg) with a history of angina pectoris and angiographically normal coronary arteries underwent a pacing study with measurement of great cardiac vein flow, lactate and oxygen content, and left ventricular filling pressure. Compared with 28 control subjects without hypertrophic cardiomyopathy, their resting coronary blood flow was higher (91 +/- 27 vs 66 +/- 17 ml/min; p less than .001) and their coronary resistance was lower (1.13 +/- 0.38 vs 1.55 +/- 0.45 mm Hg/ml/min; p less than .001). Left ventricular end-diastolic pressure (16 +/- 6 vs 11 +/- 3 mm Hg; p less than .001) and pulmonary arterial wedge pressure (13 +/- 5 vs 7 +/- 3 mm Hg; p less than .001) were significantly higher in patients with hypertrophic cardiomyopathy. During pacing, coronary flow rose in both groups, although coronary and myocardial hemodynamics differed greatly. In contrast to the linear increase in flow in control subjects up to heart rate of 150 beats/min (66 +/- 17 to 125 +/- 28 ml/min), patients with hypertrophic cardiomyopathy demonstrated an initial rise in flow to 133 +/- 31 ml/min at an intermediate heart rate of 130 beats/min. At this point, 12 of 20 patients developed their typical chest pain. With continued pacing to a heart rate of 150 beats/min, mean coronary flow fell to 114 +/- 29 ml/min (p less than .002), with 18 of 20 patients experiencing their typical chest pain and metabolic evidence of myocardial ischemia. This fall in coronary flow was associated with a substantial rise in left ventricular end-diastolic pressure (30 +/- 9 mm Hg immediately after peak pacing). In the 14 patients whose coronary flow actually fell from intermediate to peak pacing, the rise in left ventricular end-diastolic pressure in the same interval was greater than that of the six patients whose flow remained unchanged or increased (11 +/- 8 vs 2 +/- 2 mm Hg; p less than .01). In addition, despite metabolic and hemodynamic evidence of myocardial ischemia, the arteriovenous O2 difference actually narrowed at peak pacing. Thus most patients with hypertrophic cardiomyopathy achieved maximum coronary vasodilation and flow at modest increases in heart rate. Elevation in left ventricular filling pressure, probably related to ischemia-induced changes in ventricular compliance, was associated with a decline in coronary flow.(ABSTRACT TRUNCATED AT 400 WORDS)
Assessment of short-, medium-, and long-term variations in arterial dimensions from computer-assisted quantitation of coronary cineangiograms.
Authors: Reiber J H , Serruys P W , Kooijman C J , Wijns W , Slager C J , Gerbrands J J , Schuurbiers J C , den Boer A , Hugenholtz P G
Published: June 2011

A computer-assisted technique has been developed to assess absolute coronary arterial dimensions from 35 mm cineangiograms. The boundaries of optically magnified and video-digitized coronary segments and the intracardiac catheter are defined by automated edge-detection techniques. Contour positions are corrected for pincushion distortion. The accuracy and precision of the edge detection procedure as assessed from cinefilms of contrast-filled acrylate (Perspex) models were -30 and 90 micrometers, respectively. The variability of the analysis procedure itself in terms of absolute arterial dimensions was less than 0.12 mm, and in terms of percentage arterial narrowing for coronary obstructions less than 2.74%. Short-, medium-, and long-term variability measurements were assessed from repeated coronary angiographic examinations performed 5 min, 1 hr, and 90 days apart, respectively. For all studies the mean differences in absolute diameters were less than 0.13 mm. The variability in obstruction diameter ranged from 0.22 mm for the best-controlled study (medium-term) to 0.36 mm for the least-controlled study (long-term); variability in reference diameter ranged from 0.15 to 0.66 mm, respectively. It is concluded that the biological variations are a source of major concern and that further attempts toward standardization of the angiographic procedure are seriously needed.
Lack of reflex increase in myocardial sympathetic tone after captopril: potential antianginal effect.
Authors: Daly P , Mettauer B , Rouleau J L , Cousineau D , Burgess J H
Published: June 2011

Many vasodilators have been tried as antianginal agents, but the reflex increase in sympathetic tone produced by these drugs necessitate their use with caution in patients with angina. In the first part of this study, captopril was given to 14 patients with angina and systolic arterial pressures of greater than 120 mm Hg. Over the short term, captopril decreased arterial blood pressure (from 110 +/- 18 to 98 +/- 18 mm Hg, p less than .01) without increasing heart rate (75 +/- 15 vs 74 +/- 15 beats/min), arterial concentrations of epinephrine (0.38 +/- 0.28 vs 0.34 +/- 0.25 nM) or norepinephrine (2.7 +/- 2.1 vs 2.8 +/- 2.1 nM), or transmyocardial norepinephrine balance (216 +/- 254 vs 146 +/- 170 p mol/min). Captopril decreased average myocardial oxygen consumption (9.7 +/- 4.1 to 8.2 +/- 2.7 ml/min, p less than .01). Given over the long term (mean 5.5 months), captopril decreased the severity of angina from NYHA classification 3.0 +/- 0.8 to 1.6 +/- 0.8. In the second part of this study, captopril was given in a prospective, randomized, double-blind, placebo-controlled study to 21 patients with stable exercise-induced angina and systolic arterial pressures greater than 120 mm Hg. Captopril increased exercise time (309 +/- 137 vs 374 +/- 142 sec, p less than .05) without changing anginal threshold (rate-pressure product 17.0 +/- 6.0 vs 17.1 +/- 5.6 X 10(-3)). We conclude that captopril decreases mean arterial pressure without causing a reflex increase in myocardial sympathetic tone.(ABSTRACT TRUNCATED AT 250 WORDS)
Cumulative inhibitory effect of low-dose aspirin on vascular prostacyclin and platelet thromboxane production in patients with atherosclerosis.
Authors: Weksler B B , Tack-Goldman K , Subramanian V A , Gay W A
Published: June 2011

The relationship between the antithrombotic and antiplatelet effects of aspirin is complex, since aspirin influences other systems that protect against thrombosis as well as inhibiting platelet function. We investigated possible cumulative effects of low-dose aspirin on vascular production of prostacyclin in patients with documented atherosclerotic cardiovascular disease. Candidates for coronary artery vein graft bypass ingested 20 mg of aspirin daily during the week before surgery, and platelet aggregation, platelet formation of thromboxane A2 (TXA2), aortic and saphenous vein production of prostacyclin (PGI2), and hemostatic status were measured at the time of the bypass surgery. Low-dose aspirin markedly inhibited platelet aggregation responses and reduced TXA2 generation by greater than 90%, effects similar to those observed with much higher doses of aspirin. Both aortic and saphenous vein production of PGI2 were inhibited by 50% compared with PGI2 produced by vascular tissues of control subjects who received no aspirin preoperatively (51 +/- 10 pg 6-keto-PGF1 alpha/mg aortic wet weight [mean +/- SEM] in aspirin-treated subjects vs 130 +/- 16 pg/mg in control subjects, and 71 +/- 8 pg/mg saphenous vein wet weight vs 131 +/- 17 pg/mg). Blood loss at surgery was not significantly increased by preoperative low-dose aspirin as measured by chest tube drainage (754 +/- 229 ml in aspirin-treated subjects vs 645 +/- 271 ml in control subjects), hematocrit nadir (31.2 +/- 1.9% vs 31.8 +/- 1.7%), or transfusions (2.2 +/- 1.3 units of red blood cells vs 2.2 +/- 1.7 units).(ABSTRACT TRUNCATED AT 250 WORDS)
Reduced regional myocardial perfusion in the presence of pharmacologic vasodilator reserve.
Authors: Canty J M , Klocke F J
Published: June 2011

To determine whether reductions in regional myocardial perfusion at reduced coronary arterial pressures reliably indicate maximal vasodilation of the distal vasculature, coronary autoregulation was studied in open-chest dogs at heart rates of approximately 60 beats/min, a level at which metabolic demand, time-averaged systolic compressive forces, and transmural vasodilator reserve approximate those found under usual resting conditions. Circumflex pressure was controlled with a programmable pressure source. Regional circumflex inflow was 0.56 +/- 0.04(SEM) ml . min-1 . g-1 when circumflex pressure equaled spontaneous aortic pressure and fell to 0.34 +/- 0.02 ml . min-1 . g-1 when circumflex pressure was reduced to 35 mm Hg. Reductions were similar in each myocardial layer, with endocardial flow falling from 0.68 +/- 0.04 to 0.39 +/- 0.03 ml . min-1 . g-1. During adenosine-induced vasodilation at 35 mm Hg, full-thickness and endocardial flows rose to 0.92 +/- 0.08 and 1.07 +/- 0.10 ml . min-1 . g-1, respectively. When coronary pressure was reduced to 25 mm Hg and autoregulation was again operative, full-thickness and endocardial flows fell to 0.28 +/- 0.03 and 0.28 +/- 0.04 ml . min-1 . g-1. During adenosine vasodilation at 25 mm Hg endocardial flow did not increase significantly but epicardial reserve remained present. These results indicate that significant reductions in regional myocardial perfusion can occur before pharmacologic vasodilator reserve is exhausted. In the absence of tachycardia, endocardial vasodilator reserve can persist to coronary pressures less than 35 mm Hg, but is ordinarily exhausted before epicardial vasodilator reserve.
A Doppler echocardiographic method for calculating volume flow across the tricuspid valve: correlative laboratory and clinical studies.
Authors: Meijboom E J , Horowitz S , Valdes-Cruz L M , Sahn D J , Larson D F , Oliveira Lima C
Published: June 2011

In this study we tested a two-dimensional Doppler echocardiographic method for measuring volume flow across the tricuspid valve. Five anesthetized, open-chest dogs had a calibrated electromagnetic flow probe placed on the ascending aorta. Volume flow across the tricuspid valve was controlled by creating a variable femoral-to-pulmonary arterial shunt. Since no standard plane provided a direct view of the tricuspid valve orifice, tricuspid flow area was estimated by calculating a fixed circular flow orifice from the maximal late diastolic diameter of the tricuspid anulus in a four-chamber view. Doppler-determined velocities across the tricuspid valve and tricuspid anulus images in the four-chamber view were obtained in inspiration and expiration. For 24 cardiac outputs (0.6 to 4.0 liters/min), inspiratory tricuspid flow determined by the Doppler method correlated minimally better (r = .90, SEE = 0.30 liter/min) than did expiratory measurements (r = .89, SEE = 0.35 liter/min) with the time-averaged systemic flow determined electromagnetically. Doppler-determined tricuspid volume flows in four-chamber and short-axis two-dimensional echocardiographic views from 10 children were then compared with values determined simultaneously by thermodilution during cardiac catheterization. In the children, Doppler-determined flows in short-axis and four-chamber views, both in inspiration and expiration, were similar; when results for the two views were averaged in inspiration and expiration, the tricuspid flows predicted by the Doppler method were highly correlated (r = .98, SEE = 0.48 liter/min) with the results of thermodilution. The two-dimensional Doppler echocardiographic method provides a means of estimating volume flow across the tricuspid valve noninvasively.
Assessment of myocardial ischemia with proton magnetic resonance: effects of a three hour coronary occlusion with and without reperfusion.
Authors: Johnston D L , Brady T J , Ratner A V , Rosen B R , Newell J B , Pohost G M , Okada R D
Published: June 2011

Proton (hydrogen-1) magnetic resonance imaging techniques have potential for the detection and characterization of changes associated with myocardial ischemia. Since image contrast is dependent on T1 and T2 relaxation times, we examined these parameters in a canine preparation of occlusion of the left anterior descending coronary artery. Of 16 dogs studied, seven underwent 3 hr of coronary artery occlusion and nine underwent 3 hr of occlusion followed by 1 hr of reperfusion. After the dogs were killed, the hearts of four from each group were imaged in a small bore, 1.4 tesla magnet. From all hearts myocardial segments were obtained from the normal zone and the central ischemic zone (CZ). These segments were divided into epicardial and endocardial sections and studied in a spectrometer (20 MHz). After 3 hr of occlusion, CZ endocardial T1 and T2 increased significantly (p less than .01 and p less than .05, respectively). Changes in CZ epicardial relaxation times were not as marked. Although T1 and T2 tended to be higher in the reperfused group compared with the nonreperfused group, the differences did not reach statistical significance. In keeping with the spectrometric findings, T1-dependent inversion recovery images and T2-dependent spin-echo images of the excised hearts demonstrated excellent contrast between normal and ischemic myocardium. Modest correlations were noted for both groups between blood flows during occlusion measured by the microsphere technique and T1 and T2 relaxation times. In summary, relaxation times T1 and T2 increase regionally after 3 hr of coronary artery occlusion and tend to be accentuated by reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
Proximal coronary vasomotor reactivity after exercise training in dogs.
Authors: Bove A A , Dewey J D
Published: June 2011

The effects of exercise on large coronary vasoreactivity were determined in eight dogs trained by treadmill running for 8 weeks. Six nontrained dogs comprised the control group. The trained group showed a significant reduction in heart rate during graded submaximal exercise testing when compared with the controls, and resting plasma levels of norepinephrine (nontrained group, 331 +/- 99 pg/ml; trained group, 142 +/- 30 pg/ml; p less than .05) and epinephrine (nontrained, 424 +/- 105; trained, 258 +/- 45 pg/ml; p less than .05) were reduced significantly in the trained group. Epicardial coronary responses to intracoronary infusion of serotonin and phenylephrine were evaluated by quantitative coronary angiography, and myocardial blood flow was measured with 15 microns radioactive microspheres. Left ventricular/body weight ratio was similar in the trained (4.81 +/- 0.24 g/kg) and nontrained groups (4.79 +/- 0.17), and no differences were noted in resting myocardial oxygen consumption or coronary arteriovenous oxygen difference. The constriction of the proximal left anterior descending artery (LAD) in response to serotonin infusion was not different in the two groups, but the LAD and circumflex artery constrictor responses to phenylephrine were attenuated in the trained when compared with the nontrained dogs. The data indicate that endurance exercise diminishes the large epicardial coronary vasoconstrictor response to alpha-adrenergic stimulation, but not to serotonin. The blunted constrictor response in the trained animals suggests that exercise may be useful in reducing epicardial coronary vasoconstriction, which is thought to be important in some patients with coronary artery disease.
Unstable angina with fatal outcome: dynamic coronary thrombosis leading to infarction and/or sudden death. Autopsy evidence of recurrent mural thrombosis with peripheral embolization culminating in total vascular occlusion.
Authors: Falk E
Published: June 2011

Extensive microscopic examination of epicardial arteries and myocardium was performed in 25 cases of sudden death due to acute coronary thrombosis. Eighty-one percent of the thrombi had a layered structure with thrombus material of differing age, indicating that they were formed successively by repeated mural deposits that caused progressive luminal narrowing over an extended period of time. This episodic growth of the thrombus was accompanied by intermittent fragmentation of thrombus in 73% of the cases, with peripheral embolization causing microembolic occlusion of small intramyocardial arteries associated with microinfarcts. The period of unstable angina before the final heart attack was, in all but one of 15 patients, characterized by such an ongoing thrombotic process in a major coronary artery where recurrent mural thrombus formation seemed to have alternated with intermittent thrombus fragmentation. The culmination of this "dynamic" thrombotic process in total vascular occlusion caused the final infarction and/or sudden death.
Significance of adventitial inflammation of the coronary artery in patients with unstable angina: results at autopsy.
Authors: Kohchi K , Takebayashi S , Hiroki T , Nobuyoshi M
Published: June 2011

A quantitative analysis of adventitial inflammation of the coronary artery with intimal lesions is described in 12 patients who suffered coronary death and had had unstable angina (crescendo angina) at rest (group 1). After autopsy in these patients we examined epon-embedded cross sections by light and electron microscopy, paying particular attention to the adventitia, and compared these results with those in six patients who had had angina but died of noncardiac causes (group 2) and those in 22 patients who did not have angina (group 3). Of the 132 segments from group 1 patients, 39 (30%) were narrowed 76% to 100% by atherosclerotic plaque (group 2, 27%; group 3, 1%), and 23 (17%) had occlusive thrombi. Of the 264 sections (two from each segment) from group 1 that were examined, 98 (37%) (group 2, 15%; group 3, 9%) revealed clustered infiltration of inflammatory cells in the adventitia, half of which were associated with vascular nerve involvement. These findings in the adventitia may be related to the vasospastic component of unstable angina.
Digital subtraction fluoroscopy: a new method of detecting coronary calcifications with improved sensitivity for the prediction of coronary disease.
Authors: Detrano R , Markovic D , Simpfendorfer C , Franco I , Hollman J , Grigera F , Stewart W , Ratcliff N , Salcedo E E , Leatherman J
Published: June 2011

The association between calcification of the coronary arteries and coronary artery narrowing is well established. However, fluoroscopic visualization of coronary calcifications has been insufficiently sensitive to be useful as a screening test. Since digitization of radiographic images permits the subtraction of noncardiac structures from moving cardiac structures, such subtraction might increase the sensitivity of coronary fluoroscopy. To determine whether coronary calcifications were better visualized with digital subtraction fluoroscopy than with conventional fluoroscopy, we taped diseased human coronary arteries to a pulsating water balloon inside the thorax of a dog cadaver and studied this model with both fluoroscopic techniques. Calcific atherosclerotic plaques were more easily identified with digital subtraction fluoroscopy than with conventional fluoroscopy. We tested the method clinically by submitting 191 subjects without history or electrocardiographic evidence of previous myocardial infarction who were referred for coronary arteriography to both fluoroscopic studies. For at least one, at least two, and three calcified coronary arteries, digital fluoroscopy was more sensitive (92%, 66%, and 40%) than conventional fluoroscopy (63%, 21%, and 2%) (all p less than .001) for the prediction of significant coronary obstructions (greater than 50%). Although digital fluoroscopy was less specific than conventional fluoroscopy (digital: 65%, 89%, and 97%; conventional: 81%, 98%, and 100%) (all but last, p less than .01), receiver operating curve analysis revealed a significantly larger area under the curve, indicating higher accuracy for the digital technique (p = .03). Digital subtraction fluoroscopy was more accurate in younger than in older patients.(ABSTRACT TRUNCATED AT 250 WORDS)
Assessment of fibrosis in infarcted human hearts by analysis of ultrasonic backscatter.
Authors: Hoyt R H , Collins S M , Skorton D J , Ericksen E E , Conyers D
Published: June 2011

In animal hearts, the magnitude of integrated ultrasonic backscatter is increased in fibrotic myocardium. Our purpose in this study was to quantitate the relationship between ultrasonic backscatter and collagen deposition in 10 excised human hearts with old infarcts. A 2.25 MHz, 50% fractional bandwidth transducer was positioned at the transducer focal distance from the epicardium of each specimen. The radio frequency backscatter signal was digitized, squared, and integrated to yield the integrated ultrasonic backscatter, which was referenced to the backscatter from a water/steel interface. The interrogated myocardium was then excised and divided into two portions. One portion was assayed for hydroxyproline, a marker for collagen. A second portion was sectioned, stained with Masson's trichrome, and studied with the use of a computer-assisted image analysis system. There was a linear correlation between the magnitude of integrated backscatter and myocardial collagen content estimated by hydroxyproline assay (r = .78). Quantitative histologic analysis revealed a variable relationship between the transmural distribution of collagen and the corresponding transmural pattern of the backscatter signal. In two specimens exhibiting a discrete layer of subendocardial fibrosis, the backscatter amplitude was also increased in the subendocardial region. In specimens with other patterns of fibrosis, the local backscatter amplitude did not correspond to the transmural pattern of collagen distribution. We conclude that the quantitative analysis of ultrasonic backscatter shows promise for the noninvasive evaluation of myocardial fibrosis after infarction.