bluuebunny/crossref_metadata_2025_split huggingface dataset:
Echocardiographic detection of coronary artery disease during dobutamine infusion.
Authors: Sawada S G , Segar D S , Ryan T , Brown S E , Dohan A M , Williams R , Fineberg N S , Armstrong W F , Feigenbaum H 
Published: June 2012

BACKGROUND
Two-dimensional echocardiography performed during dobutamine infusion has been proposed as a potentially useful method for detecting coronary artery disease. However, the safety and diagnostic value of dobutamine stress echocardiography has not been established.

METHODS AND RESULTS
In this study, echocardiograms were recorded during step-wise infusion of dobutamine to a maximum dose of 30 micrograms/kg/min in 103 patients who also underwent quantitative coronary angiography. The echocardiograms were digitally stored and displayed in a format that allowed simultaneous analysis of rest and stress images. Development of a new abnormality in regional function was used as an early end point for the dobutamine infusion. No patient had a symptomatic arrhythmia or complications from stress-induced ischemia. Significant coronary artery disease (greater than or equal to 50% diameter stenosis) was present in 35 of 55 patients who had normal echocardiograms at rest. The sensitivity and specificity of dobutamine-induced wall motion abnormalities for coronary artery disease was 89% (31 of 35) and 85% (17 of 20), respectively. The sensitivity was 81% (17 of 21) in those with one-vessel disease and 100% (14 of 14) in those with multivessel or left main disease. Forty-one of 48 patients with abnormal echocardiograms at baseline had localized rest wall motion abnormalities. Fifteen had coronary artery disease confined to regions that had abnormal rest wall motion, and 26 had disease remote from these regions. Thirteen of 15 patients (87%) without remote disease did not develop remote stress-induced abnormalities, and 21 of 26 (81%) who had remote disease developed corresponding abnormalities.

CONCLUSIONS
Echocardiography combined with dobutamine infusion is a safe and accurate method for detecting coronary artery disease and for predicting the extent of disease in those who have localized rest wall motion abnormalities.
Evidence for reduced fibrinolytic activity in unstable angina at rest. Clinical, biochemical, and angiographic correlates.
Authors: Zalewski A , Shi Y , Nardone D , Bravette B , Weinstock P , Fischman D , Wilson P , Goldberg S , Levin D C , Bjornsson T D 
Published: June 2012

BACKGROUND
The goal of this study was to evaluate the role of the fibrinolytic system in patients with unstable angina at rest associated with transient electrocardiographic changes.

METHODS AND RESULTS
Tissue plasminogen activator activity in plasma was comparable among patients with unstable angina (n = 17), patients with stable exertional angina (n = 10), and control patients with normal coronary arteriograms (n = 8). In contrast, plasminogen activator inhibitor-1 (PAI-1) activity in plasma was elevated in the unstable angina group (21.67 +/- 9.52 AU/ml) as compared with either the stable angina group (12.01 +/- 7.06 AU/ml, p less than 0.02) or the controls (12.49 +/- 8.54 AU/ml, p less than 0.02). Coronary angiography performed within 24 hours after the last anginal episode showed a similar extent of coronary artery disease in the unstable and stable angina groups. However, intracoronary thrombi were observed in eight patients in the unstable angina group while no thrombus was noted in the stable angina group (chi 2 = 7.22, p less than 0.01).

CONCLUSIONS
We conclude that patients with unstable angina at rest have a reduced fibrinolytic activity and an increased incidence of intracoronary thrombi. It is postulated that elevated PAI-1 activity in the presence of coronary arterial wall injury may be an important factor leading to the development of acute coronary syndromes.
Doppler echocardiographic assessment of fetal descending aortic and umbilical blood flows. Validation studies in fetal lambs.
Authors: Schmidt K G , Di Tommaso M , Silverman N H , Rudolph A M 
Published: June 2012

BACKGROUND
Doppler ultrasound has been used to assess abdominal aortic and umbilical blood flows in the human fetus, but the accuracy of this approach has not been demonstrated in an animal model.

METHODS AND RESULTS
We compared abdominal aortic and umbilical blood flows determined by Doppler echocardiography in 12 fetal lambs with invasive flow measurements using radionuclide-labeled microspheres and electromagnetic flow transducers. We varied fetal blood flow from 100 to 950 ml/min in the abdominal aorta and from 130 to 610 ml/min in the umbilical vein. Invasive and Doppler echocardiographic flow measurements correlated well at both sites (y = 68 + 1.02x, r = 0.94, and y = 33 + 1.1x, r = 0.91, respectively). A slight overestimation of flow using the Doppler method may require a correction factor to assess actual flow. The degree of overestimation was not systematically related to measurements taken in smaller vessels or at larger angles of incidence.

CONCLUSIONS
The present study demonstrates that determination of abdominal aortic and umbilical venous flows by echocardiography and pulsed Doppler ultrasound is feasible. Doppler measurements appear to be suited to serial comparison of actual flow.
QTc prolongation measured by standard 12-lead electrocardiography is an independent risk factor for sudden death due to cardiac arrest.
Authors: Algra A , Tijssen J G , Roelandt J R , Pool J , Lubsen J 
Published: June 2012

BACKGROUND
QTc prolongation has been implicated as a risk factor for sudden death; however, a controversy exists over its significance.

METHODS AND RESULTS
In the Rotterdam QT Project, 6,693 consecutive patients who underwent 24-hour ambulatory electrocardiography were followed up for 2 years; of these, 245 patients died suddenly. A standard 12-lead electrocardiogram and clinical data at the time of 24-hour ambulatory electrocardiography were collected for all patients who died suddenly and for a random sample of 467 patients from the study cohort. In all patients without an intraventricular conduction defect (176 patients who died suddenly and 390 patients from the sample), QT interval duration was measured in leads I, II, and III and corrected for heart rate with Bazett's formula (QTc). In patients without evidence of cardiac dysfunction (history of symptoms of pump failure or an ejection fraction less than 40%), QTc of more than 440 msec was associated with a 2.3 times higher risk for sudden death compared with a QTc of 440 msec or less (95% confidence interval: 1.4, 3.9). In contrast, in patients with evidence of cardiac dysfunction, the relative risk of QTc prolongation was 1.0 (0.5, 1.9). Adjustment for age, gender, history of myocardial infarction, heart rate, and the use of drugs did not alter these relative risks.

CONCLUSIONS
These data indicate that in patients without intraventricular conduction defects and cardiac dysfunction, QTc prolongation measured from the standard electrocardiogram is a risk factor for sudden death independent of age, history of myocardial infarction, heart rate, and drug use. In patients with cardiac dysfunction, QTc duration is not related to the risk for sudden death.
Determinants of 2-year outcome after coronary angioplasty in patients with multivessel disease on the basis of comprehensive preprocedural evaluation. Implications for patient selection. The Multivessel Angioplasty Prognosis Study Group.
Authors: Ellis S G , Cowley M J , DiSciascio G , Deligonul U , Topol E J , Bulle T M , Vandormael M G 
Published: June 2012

BACKGROUND
To assess the likelihood of intermediate-term event-free survival (freedom from death, coronary artery bypass surgery, and myocardial infarction) in patients with multivessel coronary disease undergoing coronary angioplasty, 350 consecutive patients from four clinical sites were carefully evaluated and followed for 22 +/- 10 months.

METHODS AND RESULTS
Eight clinical variables were evaluated at the clinical sites, and 23 angiographic variables describing the number, morphology, and topography of coronary stenoses were evaluated at a core angiographic laboratory. Most patients had Canadian Cardiovascular Society class III or IV angina (72%), two-vessel coronary disease (68%), and well-preserved left ventricular function (mean ejection fraction, 58 +/- 12%; range, 18-85%). Follow-up was complete in 99% of patients. At 2 years, event-free survival was 72%, overall survival was 96%, freedom from bypass surgery was 82%, and freedom from nonfatal myocardial infarction without surgery was 96%. Sequential Cox proportional hazards regression analyses allowing stepwise entry of variables prospectively coded as simple, as of intermediate complexity, or as complex found event-free survival to be independently predicted by low Canadian Cardiovascular Society angina class, no diabetes, no proximal left anterior descending stenoses, and the sum of stenosis simplified risk-territory scores of 15 or less. In the absence of class IV angina and these risk factors, 2-year event-free survival was 87% and overall survival was 100%. In the presence of two or more of these risk factors, event-free survival was less than 50%.

CONCLUSIONS
Recognition of risk factors for poor long-term outcome in this setting may improve clinical decision making and provide a framework on which to base meaningful subgroup analyses in randomized trials assessing the efficacy of coronary angioplasty.
Long-term results after balloon pulmonary valvuloplasty.
Authors: McCrindle B W , Kan J S 
Published: June 2012

BACKGROUND
The objective of this study was to determine the long-term outcome of patients after percutaneous balloon pulmonary valvuloplasty (BPV) treatment of congenital pulmonary valve stenosis.

METHODS AND RESULTS
This study represents a case series with duration (mean +/- SD) of follow-up of 4.6 +/- 1.9 years. Forty-six patients with a median age of 4.6 years (range, 3 months to 56 years) had BPV at one academic institution between June 1981 and December 1986. Mean peak systolic pressure gradients from the right ventricle to the pulmonary artery were as follows: before BPV, 70 +/- 36 mm Hg; immediately after BPV, 23 +/- 14 mm Hg; at intermediate follow-up by cardiac catheterization or Doppler echocardiography at less than 2 years after BPV, 23 +/- 16 mm Hg (n = 33); and at long-term follow-up by Doppler at more than 2 years after BPV, 20 +/- 13 mm Hg (n = 42). BPV acutely reduced the gradient to less than 36 mm Hg for 41 of 46 (89%) patients. Available gradients at long-term follow-up were less than 36 mm Hg for 36 of 42 (86%) patients without additional procedures. A patient age of less than 2 years at the initial BPV was a significant risk factor for gradients over 36 mm Hg at follow-up.

CONCLUSIONS
BPV provides long-term relief of pulmonary valvular obstruction in the majority of patients. Close follow-up of patients who require BPV at less than 2 years of age is warranted.
Oxidized low density lipoproteins inhibit relaxations of porcine coronary arteries. Role of scavenger receptor and endothelium-derived nitric oxide.
Authors: Tanner F C , Noll G , Boulanger C M , Lüscher T F 
Published: June 2012

BACKGROUND
We studied the effects of low density lipoprotein (LDL) on endothelium function.

METHODS AND RESULTS
Porcine epicardial and intramyocardial coronary arteries suspended in organ chambers for isometric tension recording were exposed to LDL for 2 hours and were then washed. In epicardial coronary arteries, oxidized LDL (30-300 micrograms/ml) but not native LDL or lysolecithin inhibited endothelium-dependent relaxations to serotonin, thrombin, and aggregating platelets (5,000-75,000/microliter). Endothelium-dependent relaxations to bradykinin and A23187 and endothelium-independent relaxations to SIN-1 were unaffected by oxidized LDL. In intramyocardial coronary arteries, oxidized LDL had no appreciable effect on relaxations to serotonin. The effect of oxidized LDL on the response to serotonin in epicardial coronary arteries was completely prevented by dextran sulfate (10 micrograms/ml). The inhibitory effect of oxidized LDL persisted in the presence of pertussis toxin. Similar to the lipoproteins, L-NG-monomethyl arginine (L-NMMA) reduced relaxations to serotonin but not to bradykinin in epicardial coronary arteries. In the presence of L-NMMA, oxidized LDL further reduced the response to serotonin. In arteries in which relaxations to serotonin were inhibited by oxidized LDL, L-arginine but not D-arginine induced a full relaxation. Pretreatment with L-arginine potentiated relaxations to serotonin in arteries exposed to oxidized LDL.

CONCLUSIONS
Thus, oxidized LDL activates the scavenger receptor on endothelial cells and inhibits the receptor-operated nitric oxide formation in epicardial but not in intramyocardial coronary arteries. The mechanism is not related to dysfunction of a Gi protein but is related to a reduced intracellular availability of L-arginine. The reduced nitric oxide formation at sites of early atherosclerotic lesions may favor platelet aggregation and vasospasm, both of which are known clinical events in patients with coronary artery disease.
Mechanism of coronary vasodilation produced by bradykinin.
Authors: Pelc L R , Gross G J , Warltier D C 
Published: June 2012

BACKGROUND
Bradykinin has been demonstrated to be an endothelium-dependent vasodilator in the cerebral circulation of the mouse, but the actions of bradykinin on regional tissue perfusion in the canine coronary circulation have not been studied.

METHODS AND RESULTS
The mechanism of coronary vasodilation by bradykinin was studied in open-chest, anesthetized dogs. The role of cyclooxygenase stimulation, bradykinin B2 receptor activation, and endothelium-derived relaxing factor in bradykinin-mediated vasodilation was studied in separate groups of dogs. Bradykinin was infused intracoronarily so as to avoid changes in systemic hemodynamics capable of altering the regional distribution of coronary blood flow (radioactive microspheres). Bradykinin produced a preferential increase in subendocardial blood flow. Pretreatment with indomethacin had no effect on bradykinin-mediated increases in total left ventricular flow or the transmural distribution of coronary blood flow. Blockade of bradykinin B2 receptors with the competitive antagonist [Thi5,8, D-Phe7]-bradykinin attenuated both the increase in total flow and redistribution of perfusion to the subendocardium produced by bradykinin. Inhibition of endothelium-derived relaxing factor with quinacrine, occlusion/reperfusion, or NG-monomethyl L-arginine attenuated the total increase in left ventricular flow and blocked the redistribution of flow to the subendocardium produced by bradykinin.

CONCLUSIONS
The present results demonstrate that intracoronary infusion of bradykinin produces a preferential increase in blood flow to the subendocardium via stimulation of B2 receptors and the release of an endothelium-dependent relaxing factor that may be nitric oxide.
HDL, HDL2, and HDL3 subfractions, and the risk of acute myocardial infarction. A prospective population study in eastern Finnish men.
Authors: Salonen J T , Salonen R , Seppänen K , Rauramaa R , Tuomilehto J 
Published: June 2012

BACKGROUND
We investigated the association of cholesterol concentrations in serum high density lipoprotein (HDL) and its subfractions HDL2 and HDL3 with the risk of acute myocardial infarction in 1,799 randomly selected men 42, 48, 54, or 60 years old.

METHODS AND RESULTS
Baseline examinations in the Kuopio Ischaemic Heart Disease Risk Factor Study were done during 1984-1987. In Cox multivariate survival models adjusted for age and examination year, serum HDL cholesterol of less than 1.09 mmol/l (42 mg/dl) was associated with a 3.3-fold risk of acute myocardial infarction (95% confidence intervals [CI], 1.7-6.4), serum HDL2, cholesterol of less than 0.65 mmol/l (25 mg/dl) was associated with a 4.0-fold risk of acute myocardial infarction (95% CI, 1.9-8.3), and serum HDL3 cholesterol of less than 0.40 mmol/l (15 mg/dl) was associated with a 2.0-fold (95% CI, 1.1-4.0) risk of acute myocardial infarction. Adjustments for obesity, ischemic heart disease, other cardiovascular disease, maximal oxygen uptake, systolic blood pressure, antihypertensive medication, serum low density lipoprotein cholesterol, and triglyceride concentrations reduced the excess risks associated with serum HDL, HDL2, and HDL3 cholesterol in the lowest quartiles by 52%, 48%, and 41%, respectively. Additional adjustments for alcohol consumption, cigarettes smoked daily, smoking years, and leisure time energy expenditure reduced these excess risks associated with low HDL, HDL2, and HDL3 cholesterol levels by another 26%, 24% and 21%, respectively.

CONCLUSIONS
Our data confirm that both total HDL and HDL2 levels have inverse associations with the risk of acute myocardial infarction and may thus be protective factors in ischemic heart disease, whereas the role of HDL3 remains equivocal.
Effect of diltiazem on symptomatic and asymptomatic episodes of ST segment depression occurring during daily life and during exercise.
Authors: Théroux P , Baird M , Juneau M , Warnica W , Klinke P , Kostuk W , Pflugfelder P , Lavallée E , Chin C , Dempsey E 
Published: June 2012

BACKGROUND
Silent myocardial ischemia is an adverse prognostic marker in patients with coronary disease; however, controlled data on the effect of treatment are sparse and contradictory, and the relations among the occurrence of ST segment depression, drug efficacy, and heart rate are unclear.

METHODS AND RESULTS
Sixty patients with stable coronary artery disease, a positive treadmill exercise test and asymptomatic ST segment depression on ambulatory electrocardiographic recording were assessed in a multicenter, double-blind, placebo-controlled, cross-over trial. Treadmill exercise tests and 72-hour electrocardiographic recordings were obtained at the end of two 2-week treatment periods with sustained-release diltiazem 180 mg b.i.d. or equivalent placebo. Episodes of asymptomatic ST depression decreased by 50% or more in 70% of the patients from a median number of 4.5 (range, 0-19) to 1.5 (range, 0-13) (p = 0.0001); their cumulative duration also decreased from 78.5 (range, 0-60) to 24.5 (range, 0-411) minutes (p = 0.001). No circadian variation was found in the efficacy of diltiazem. The occurrence of ischemic type ST segment depression was modulated by changes in heart rate rather than by absolute heart rate. Diltiazem also improved exercise test end points but to a lesser extent. Time to ST segment depression increased to 341 +/- 148 from 296 +/- 154 seconds (p = 0.005). Although less frequent with diltiazem administration (45 versus 54 patients, p less than 0.03), exercise-induced ST depression was more often asymptomatic (98% versus 72% of patients, p less than 0.0001).

CONCLUSIONS
Diltiazem reduces the frequency and severity of ischemic type ST depression in patients with stable coronary artery disease.
Hemodynamic effects of octreotide in patients with autonomic neuropathy.
Authors: Hoeldtke R D , Davis K M , Joseph J , Gonzales R , Panidis I P , Friedman A C 
Published: June 2012

BACKGROUND
The somatostatin analogue, ectrootide, is being used to treat postprandial hypotension in patients with autonomic neuropathy. Although the therapeutic effect of the drug is presumably secondary to a splanchnic vasoconstrictor action, its effect on splanchnic hemodynamics has never been characterized in patients with autonomic neuropathy. Moreover, it is unknown whether octreotide acts on other vascular beds in this group of patients or whether it affects cardiac output. We, therefore, measured splanchnic, forearm, and systemic vascular resistance and cardiac output before and after administering octreotide (0.4 microgram/kg s.c.) to patients with idiopathic autonomic neuropathy and diabetic autonomic neuropathy.

METHODS AND RESULTS
Splanchnic blood flow was determined from the clearance of indocyanine green in seven patients. We observed that octreotide decreased splanchnic blood flow (from 850 +/- 77 to 664 +/- 48 ml/min, p less than 0.005), increased mean blood pressure (from 97 +/- 6 to 115 +/- 3 mm Hg, p less than 0.005), and increased splanchnic vascular resistance (from 0.118 +/- 0.012 to 0.18 +/- 0.018 mm Hg/ml/min, p less than 0.005). Forearm blood flow was measured by plethysmography in 13 patients. Octreotide increased forearm vascular resistance in patients with idiopathic autonomic neuropathy (n = 8) from 19.1 +/- 1.0 to 27.2 +/- 3.8 mm Hg/ml/min/100 ml forearm volume (p less than 0.01) and from 25.2 +/- 3.9 to 41.0 +/- 6.8 mm Hg/ml/min/100 ml (p less than 0.01) in patients with diabetic autonomic neuropathy (n = 5). Cardiac output was measured by two-dimensional echocardiography. Octreotide administration increased cardiac output in five of six patients with idiopathic autonomic neuropathy (from 4.4 +/- 0.4 to 5.0 +/- 0.5 l/min, p less than 0.02) and five of five patients with diabetic autonomic neuropathy (from 3.8 +/- 0.4 to 5.1 +/- 0.4 l/min, p less than 0.02). Systemic vascular resistance increased in patients with idiopathic autonomic neuropathy from 21.2 +/- 2 to 24.9 +/- 2.6 (p less than 0.05) but did not change in patients with diabetic autonomic neuropathy.

CONCLUSION
The pressor effect of octreotide in patients with autonomic neuropathy is associated with increased splanchnic and forearm vascular resistance and with increased cardiac output.
Effective thrombolysis without marked plasminemia after bolus intravenous administration of vampire bat salivary plasminogen activator in rabbits.
Authors: Gardell S J , Ramjit D R , Stabilito I I , Fujita T , Lynch J J , Cuca G C , Jain D , Wang S P , Tung J S , Mark G E 
Published: June 2012

BACKGROUND
The use of recombinant tissue-type plasminogen activator (t-PA) in thrombolytic therapy is frequently associated with significant fibrinogenolysis. In contrast, recombinant vampire bat salivary plasminogen activator (Bat-PA) displays strict fibrin specificity, an attribute that could be desirable in a fibrinolytic agent.

METHODS AND RESULTS
The efficacy and fibrin selectivity of Bat-PA was evaluated and compared with that of t-PA using a rabbit model of femoral arterial thrombosis. Administration of 8.1, 14, and 42 nmol Bat-PA/kg by bolus intravenous injection restored flow in 50%, 75%, and 80% of the rabbits, respectively. The incidence of reperfusion after bolus intravenous injection of 14 and 42 nmol t-PA/kg was 15% and 78%, respectively. The maximal femoral artery reperfusion flows were equivalent after treatment with 42 nmol Bat-PA/kg or 42 nmol t-PA/kg, but the time to reach maximal flow for Bat-PA was approximately one half that of t-PA. Furthermore, the rapid restoration of flow by 42 nmol Bat-PA/kg, in contrast to equimolar t-PA, was accomplished without fibrinogenolysis and with only small decreases in the plasminogen and alpha 2-antiplasmin levels. Equipotent doses of Bat-PA and t-PA both resulted in approximate 2.5-fold increases in the template bleeding times of aspirin-pretreated rabbits. The clearance of Bat-PA from rabbits exhibited biexponential elimination kinetics; approximately 80% was cleared by the relatively slow beta phase (half-life of 17.1 minutes). Overall, Bat-PA was cleared approximately fourfold slower than t-PA.

CONCLUSIONS
Bolus intravenous administration of Bat-PA would facilitate prompt initiation of thrombolytic therapy, and the avoidance of plasminemia could result in fewer and less severe bleeding complications.