bluuebunny/crossref_metadata_2025_split huggingface dataset:
Symptoms of anxiety and risk of coronary heart disease. The Normative Aging Study.
Authors: Kawachi I , Sparrow D , Vokonas P S , Weiss S T 
Published: June 2012

BACKGROUND
Several studies have suggested an increased risk of fatal coronary heart disease (CHD) among patients with panic disorder, phobic anxiety, and other anxiety disorders. We prospectively examined this association in the Normative Aging Study.

METHODS AND RESULTS
An anxiety symptoms scale was constructed out of five items from the Cornell Medical Index, which was administered to the cohort at baseline. During 32 years of follow-up, we observed 402 cases of incident coronary heart disease (137 cases of nonfatal myocardial infarction, 134 cases of angina pectoris, and 131 cases of fatal CHD: made up of 26 cases of sudden cardiac death and 105 cases of nonsudden death). A nested case-control design (involving 1869 control subjects who remained free of diagnosed CHD) was used to assess the association between anxiety and risk of CHD. Compared with men reporting no symptoms of anxiety, men reporting two or more anxiety symptoms had elevated risks of fatal CHD (age-adjusted odds ratio [OR] = 3.20, 95% confidence interval [CI]: 1.27 to 8.09), and sudden death (age-adjusted OR = 5.73, 95% CI: 1.26 to 26.1). The multivariate OR after adjusting for a range of potential confounding variables was 1.94 (95% CI: 0.70-5.41) for fatal CHD and 4.46 (95% CI: 0.92-21.6) for sudden death. No excess risks were found for nonfatal myocardial infarction or angina.

CONCLUSIONS
These data suggest an association between anxiety and fatal coronary heart disease, in particular, sudden cardiac death.
Randomized comparison of rescue angioplasty with conservative management of patients with early failure of thrombolysis for acute anterior myocardial infarction.
Authors: Ellis S G , da Silva E R , Heyndrickx G , Talley J D , Cernigliaro C , Steg G , Spaulding C , Nobuyoshi M , Erbel R , Vassanelli C 
Published: June 2012

BACKGROUND
When used in the setting of acute myocardial infarction, intravenous thrombolytic agents fail to achieve early infarct artery patency in 15% to 50% of patients. We tested the hypothesis that immediate balloon angioplasty applied to patients with failed early reperfusion would improve left ventricular function and clinical outcome at 30 days compared with conservative management alone.

METHODS AND RESULTS
One hundred fifty-one patients with first anterior wall infarction treated with any accepted intravenous thrombolytic regimen and angiographically demonstrated to have an occluded infarct vessel within 8 hours of chest pain onset were randomized to aspirin, heparin, and coronary vasodilators (conservative therapy) or to this therapy and balloon angioplasty supplemented by further thrombolytic therapy as needed. Left ventricular function was assessed using multiple-gated equilibrium radionuclide technique to determine ejection fraction, and adverse clinical outcome was assessed evaluating death, ventricular tachycardia, and class III or IV heart failure at 30 days. Seventy-three patients were randomized to conservative therapy and 78 to angioplasty. The two groups were well balanced for patient age (59 +/- 11 years), sex (82% were male), and time to randomization (4.5 +/- 1.9 hours). Angioplasty was technically successful in 72 of 78 randomized patients (92%). Two patients randomized to conservative therapy crossed over to angioplasty within 72 hours. Resting 30-day ejection fraction was 40 +/- 11% in the angioplasty group and 39 +/- 12% in the conservative group (P = .49), but ejection fraction with exercise was 43 +/- 15% and 38 +/- 13% for the angioplasty and conservatively treated groups, respectively (P = .04). Adverse clinical outcomes included death in 5% and 10% (P = .18), severe heart failure in 1% and 7% (P = .11), and either death or severe heart failure in 6% and 17% (P = .05) of the angioplasty and conservatively managed groups, respectively.

CONCLUSIONS
When applied to patients with first anterior infarction, rescue angioplasty appears to be useful in the prevention of death or severe heart failure, with improvement in exercise, but not resting, ejection fraction. This strategy deserves further study and highlights the potential advantage of early mechanical restoration of infarct vessel patency when thrombolytic therapy has failed.
Use of Hirulog in the prevention of venous thrombosis after major hip or knee surgery.
Authors: Ginsberg J S , Nurmohamed M T , Gent M , MacKinnon B , Sicurella J , Brill-Edwards P , Levine M N , Panju A A , Powers P , Stevens P 
Published: June 2012

BACKGROUND
The study objective was to determine whether Hirulog, a direct thrombin inhibitor, has potential efficacy and safety in the prevention of deep vein thrombosis (DVT) in orthopedic patients. A phase 2 open-label, dose-escalating design was used to study 222 unselected patients undergoing major hip or knee surgery in tertiary-care, university-affiliated hospitals.

METHODS AND RESULTS
Subcutaneous Hirulog was initiated postoperatively. Patients were evaluated for bleeding and symptomatic pulmonary embolism, and mandatory bilateral venography was performed before discharge. Dose escalations were made on the basis of observed rates of bleeding and venous thrombosis. There were five dosage regimens used: 0.3 mg/kg every 12 hours, 0.6 mg/kg every 12 hours, 1.0 mg/kg every 12 hours for 3 days followed by 0.6 mg/kg every 12 hours for up to 11 days, 1.0 mg/kg every 12 hours, and 1.0 mg/kg every 8 hours. One hundred seventy-seven patients who had technically adequate bilateral venography or objectively documented pulmonary embolism were included in the primary analysis of efficacy. The highest dosage regimen (1.0 mg/kg every 8 hours) provided the lowest rates of total DVT (17%) and proximal DVT (2%), both of which were significantly lower (P = .010 and P = .023, respectively) than the pooled rates of total (43%) and proximal (20%) DVT seen with the first four regimens. Bleeding rates were low (< 5%) with all regimens.

CONCLUSIONS
This study demonstrates that 1.0 mg/kg Hirulog every 8 hours started postoperatively is potentially efficacious and safe for the prevention of DVT after major hip or knee surgery.
Thrombolytic effects of recombinant fibrolase or APSAC in a canine model of carotid artery thrombosis.
Authors: Markland F S , Friedrichs G S , Pewitt S R , Lucchesi B R 
Published: June 2012

BACKGROUND
Thrombolytic agents used clinically rely on the activation of plasminogen to plasmin. Plasmin possesses multiple actions including increasing thrombin activity and activation of platelets. Thus, after successful thrombolytic therapy, arterial hyperactivity and reocclusion may be the result of a predominant plasmin-induced thrombogenic action at the site of the residual thrombus. Fibrolase, a direct-acting fibrinolytic enzyme from southern copperhead snake venom, induces rapid clot lysis in vitro. Fibrolase does not rely on plasminogen activation or any other bloodborne components for activity and is not inhibited by any of the rapidly acting serine proteinase inhibitors in blood.

METHODS AND RESULTS
We investigated the efficacy of fibrolase to lyse an occlusive thrombus formed in the carotid artery of the anesthetized dog. Electrolytic injury was initiated in both the right and left carotid arteries. Thirty minutes after both arteries were occluded, each vessel was infused with either fibrolase (4 mg/kg over 5 minutes) or physiological saline (over 5 minutes). In two separate groups of dogs, anisoylated plasminogen streptokinase activator complex (APSAC) (0.1 U/kg) was infused into the occluded vessel. In the artery infused with fibrolase, five of five dogs exhibited patency within 6 +/- 1 minutes of the infusion (P < .05 versus vehicle-treated artery; Fisher's exact test). In the contralateral carotid artery that received vehicle, the occlusion was maintained throughout the experimental protocol. APSAC alone lysed the thrombus in each vessel within 17 +/- 3 minutes. Five minutes after the end of fibrolase administration and in one of the groups administered APSAC, a glycoprotein (GP)IIb/IIIa antibody, 7E3 (0.8 mg/kg IV), was administered to prevent reocclusion of the patent artery. After 7E3 administration, the vessel treated with fibrolase remained patent in four of five dogs, and six of six APSAC-treated vessels were patent for the remainder of the observation period (2 hours).

CONCLUSIONS
These studies demonstrate that local administration of fibrolase lyses a carotid arterial thrombus rapidly without excessive hemorrhage or hemodynamic compromise. The enzyme in combination with antiplatelet therapy (7E3) offers a unique mechanism for clot dissolution and may prove useful as a clinically efficacious alternative to presently used thrombolytic agents or may act in a synergistic manner with plasminogen activators.
Acute effects of nitrates on exercise testing in patients with syndrome X. Clinical and pathophysiological implications.
Authors: Lanza G A , Manzoli A , Bia E , Crea F , Maseri A 
Published: June 2012

BACKGROUND
Sublingual nitrates are much more effective in relieving angina pectoris in patients with coronary artery disease than in patients with syndrome X, but it is not known whether their effect on exercise tolerance is also different in these two groups of patients.

METHODS AND RESULTS
Treadmill exercise testing was performed before and after administration of sublingual isosorbide dinitrate (ISDN, 5 mg) in 18 patients with syndrome X (effort angina and normal coronaries, group X) and in 33 patients with documented coronary artery disease (group C). As a selection criterion, all patients had ST-segment depression > or = 1 mm on the control exercise test. Compared with the control test, the main differences in the two groups observed during the exercise test after administration of ISDN were (1) heart rate at 1-mm ST-segment depression was higher (126 +/- 25 versus 104 +/- 15 beats per minute [bpm], P < .01) in group C, whereas it was not different (125 +/- 15 versus 126 +/- 16 beats per minute) in group X; (2) the rate-pressure product at 1-mm ST-segment depression, the time to 1-mm ST-segment depression, and the exercise duration were significantly improved in group C (P < .01 for all) but were worsened in group X (18,047 +/- 4159 versus 20,535 +/- 4507 bpm . mm Hg, P = .014; 268 +/- 312 versus 429 +/- 214 seconds, P < .01; 494 +/- 279 versus 622 +/- 194 seconds, P = .013, respectively); (3) a normalization of the ECG (no ST-segment depression) was obtained in 10 patients (30%) of group C but in only 1 (5%) of group X (P < .01); (4) angina was prevented in 10 of 19 patients of group C but in no patient of group X (P < .01).

CONCLUSIONS
In patients presenting with anginal chest pain, the effects of sublingual nitrates on exercise testing appear to be clinically useful to distinguish patients with coronary artery stenoses from patients with syndrome X. Indeed, worsening of exercise tolerance is highly predictive of normal coronary arteries. Furthermore, the failure of nitrates to improve exercise tolerance in patients with syndrome X suggests that a deficiency in coronary prearteriolar nitric oxide production is unlikely to play a key role in the pathophysiology of the syndrome.
Different effects of strenuous exercise and moderate exercise on platelet function in men.
Authors: Wang J S , Jen C J , Kung H C , Lin L J , Hsiue T R , Chen H I 
Published: June 2012

BACKGROUND
Platelets play an important role in the pathogenesis of cardiovascular diseases. It is also noticed that on one hand, regular exercise can reduce the risk of cardiovascular diseases, and on the other hand, vigorous exercise provokes sudden cardiac death. We therefore hypothesize that various intensities of exercise may affect platelet function differently.

METHODS AND RESULTS
Strenuous and moderate exercise (about 50% to 55% of peak oxygen consumption, VO2peak) on a bicycle ergometer in 10 sedentary and 10 physically active healthy young men was executed on two separate occasions. Blood samples were collected before and immediately after exercise. A newly designed tapered parallel plate chamber was used to assess platelet adhesiveness. Platelet aggregation induced by ADP was evaluated by the percentage of reduction in single platelet count. beta-Thromboglobulin (beta-TG) and platelet factor 4 (PF4) were measured by ELISA. In addition, a similar study on 5 patients with stable angina were also conducted. Our results showed that (1) in the sedentary healthy group, platelet adhesiveness and aggregation were increased by strenuous exercise and depressed by moderate exercise; (2) in the active healthy group, platelet adhesiveness and aggregation were enhanced by severe exercise, whereas only aggregation was decreased by moderate exercise; (3) in the patients with stable angina, platelet adhesiveness and aggregation were enhanced by strenuous exercise and adhesiveness was suppressed by moderate exercise; (4) the degree of hemoconcentration induced by acute exercise tended to be related to the severity of exercise in all subjects; and (5) although severe exercise elevated beta-TG and PF4, there were no significant changes in beta-TG, PF4, and the ratio of beta-TG to PF4 in healthy subjects after exercise.

CONCLUSIONS
It is concluded that platelet adhesiveness and aggregability may be sensitized by strenuous exercise in both healthy subjects and patients with stable angina. In contrast, platelet function can be suppressed significantly by moderate exercise in the healthy and tends to be depressed in patients with stable angina. The former may increase the risk of cardiac arrest and the latter may protect us from cardiovascular diseases. In addition, the effects of acute exercise tend to be more pronounced in the sedentary than in the active.
Timing and velocity of ejection as major determinants of end-systolic pressure in isolated rabbit hearts.
Authors: Ezzaher A , el Ouazzani T , Crozatier B 
Published: June 2012

BACKGROUND
Systolic shortening is known to produce muscle deactivation. The present study was designed to analyze whether the velocity and the timing of ejection play a role on end-systolic pressure-volume relations (ESPVR).

METHODS AND RESULTS
In isolated rabbit hearts, left ventricular pressure and volume were recorded and digitized, and left ventricular volume was controlled by a servosystem (4-millisecond cycles) to alter the timing of ejection. A significant deficit in end-systolic pressure was observed when ejection was late in systole with respect to earlier ejection. This was associated with a significantly reduced end-systolic elastance. End-systolic pressure of beats with slow ejection was intermediate between that of the beats with early ejection and that of beats with late ejection with a significantly increased end-systolic volume compared with beats with early rapid ejection. The same results were obtained with hypertrophied hearts (abdominal aortic stenosis). Pressure-volume loop areas were significantly increased in beats with slow ejections and with rapid delayed ejections versus early rapid ejections. No change in the positive peak of dP/dt was observed when the timing and the velocity of ejection were modified.

CONCLUSIONS
ESPVR is modified by the ejection profile, with a decreased end-systolic pressure and an increased pressure-volume loop area related to the velocity and the amount of shortening during the end-systolic phase. These indices of ventricular function thus must be used with caution when the timing of ejection is altered, and the end-diastolic volume-peak dP/dt relation may be a better index of ventricular function.
Effect of ventilation on resuscitation in an animal model of cardiac arrest.
Authors: Idris A H , Becker L B , Fuerst R S , Wenzel V , Rush W J , Melker R J , Orban D J 
Published: June 2012

BACKGROUND
The need for ventilation during the initial management of cardiac arrest is an important public health problem that is being debated. The present study was designed to determine whether ventilation affects return of spontaneous circulation from cardiac arrest in a swine model with an interval of untreated ventricular fibrillation of 6 minutes, as reported in witnessed out-of-hospital human cardiac arrest.

METHODS AND RESULTS
Twenty-four animals were randomly assigned to two groups: one that received ventilation during the first 10 minutes of chest compression and one that did not. Coronary perfusion pressure and minute ventilation were continuously recorded. Arterial and mixed venous blood gases were measured at intervals. Return of spontaneous circulation was defined prospectively as an aortic systolic blood pressure of > 80 mm Hg for > 5 minutes and was the primary outcome variable. All animals were anesthetized, paralyzed, and intubated. Ventricular fibrillation was induced and persisted for 6 minutes without chest compression, followed by mechanical chest compression for 10 minutes and then attempted defibrillation. Animals without return of spontaneous circulation were given epinephrine, ventilation, and chest compression for an additional 3 minutes. Defibrillation was again attempted, and animals were assessed for return of spontaneous circulation. There were no significant differences between the two groups in baseline prearrest mean cardiac index, coronary perfusion pressure, or arterial and mixed venous blood gases. However, after 9 minutes of chest compression, significant differences were noted between the ventilated and nonventilated groups. The nonventilated group had significantly (P < .05) lower mean arterial PO2 (38 +/- 17 mm Hg compared with 216 +/- 104 mm Hg) and higher PCO2 (62 +/- 16 mm Hg compared with 35 +/- 8 mm Hg), lower mixed venous PO2 (15 +/- 7 mm Hg compared with 60 +/- 7 mm Hg). Nine of 12 (75%) of the ventilated animals, and only 1 of 12 (8%) of the nonventilated animals had return of spontaneous circulation after cardiac arrest (P < .002).

CONCLUSIONS
In this animal model of cardiac arrest, ventilation was important for resuscitation. The importance of ventilation could be related to the prolonged duration of untreated ventricular fibrillation and the significantly greater hypoxia and hypercarbic acidosis found in the nonventilated animals.
Selection and Treatment of Candidates for Heart Transplantation
Authors: Costanzo Maria Rosa , Augustine Sharon , Bourge Robert , Bristow Michael , O’Connell John B. , Driscoll David , Rose Eric 
Published: June 2012

Improved outcome of heart failure in response to medical therapy, coupled with a critical shortage of donor organs, makes it imperative to restrict heart transplantation to patients who are most disabled by heart failure and who are likely to derive the maximum benefit from transplantation. Hemodynamic and functional indexes of prognosis are helpful in identifying these patients.
Stratification of ambulatory heart failure patients by objective criteria, such as peak exercise oxygen consumption, has improved ability to select appropriate adult patients for heart transplantation. Such patients will have a poor prognosis despite optimal medical therapy. When determining the impact of individual comorbid conditions on a patient’s candidacy for heart transplantation, the detrimental effects of each condition on posttransplantation outcome should be weighed.
Evaluation of patients with severe heart failure should be done by a multidisciplinary team that is expert in management of heart failure, performance of cardiac surgery in patients with low left ventricular ejection fraction, and transplantation. Potential heart transplant candidates should be reevaluated on a regular basis to assess continued need for transplantation.
Long-term management of heart failure should include continuity of care by an experienced physician, optimal dosing in conventional therapy, and periodic reevaluation of left ventricular function and exercise capacity. The outcome of high-risk conventional cardiovascular surgery should be weighed against that of transplantation in patients with ischemic and valvular heart disease.
Establishment of regional specialized heart failure centers may improve access to optimal medical therapy and new promising medical and surgical treatments for these patients as well as stimulate investigative efforts to accelerate progress in this critical area.
Experimental Dissection of Media of Aorta by Pressure
Authors: Hirst Albert E. , Johns Varner J. 
Published: June 2012

The pressure required to produce intramural dissection was determined by injection of water into the media of strips of aorta obtained at postmortem examination. The mean pressure required reached a maximum in the second and third decades and decreased gradually thereafter. No differences in the pressure required was noted when comparisons were made by race, sex, different segments of the aorta, different strata of the media, or in the region of atherosclerotic lesions. Pregnancy (postpartum state) did not decrease the resistance in two instances. A slight increase in the pressure required was observed in the aortas of patients with hypertensive disease, and a marked increase was encountered in the presence of syphilitic aortitis. The resistance of the aorta in spontaneously occurring dissecting aneurysm was variable; one case had a normal resistance while the other was impaired.
The authors postulate that a solitary focus of medial degeneration strategically located is an adequate stimulus for dissection. Subsequently, rupture of vasa vasorum into this weakened area results in a rapidly expanding bleb. The pressure required to produce further enlargement of the bleb will vary inversely with its diameter, thus tending to extend the dissection. This mechanism may explain the frequent finding of an histologically normal aorta in random sections from cases with extensive intramural dissection.
Chronic Experimental Hypertension in Dogs after Constriction of Brachiocephalic and Left Subclavian Arteries
Authors: Hawthorne Edward W. , Mandal A. K. 
Published: June 2012

In summary, the studies suggest that:
(1) Simultaneous and controlled constriction of the brachiocephalic and left subclavian arteries resulted in chronic femoral hypertension in seven dogs.
(2) This hypertension is associated heniodynamically with an increase in cardiac index due mainly to an increased stroke volume.
(3) The suggestion is made that the initiating mechanism for this type of experimental hypertension is a chronic decrease in endosinal pulse pressure.
Phasic and Mean Blood Flow in the Canine Septal Artery and an Estimate of Systolic Resistance in Deep Myocardial Vessels
Authors: ECKSTEIN RICHARD W. , MOIR THOMAS W. , DRISCOL THOMAS E. 
Published: June 2012

Phasic flow in the canine septal artery was recorded with an orifice meter supplied by pulsatile aortic pressure. Flow patterns were recorded when right ventricular pressure was normal and contrasted with those following elevation of right ventricular pressure in order to minimize the dynamic effect of the superficial component of the artery. Results indicate that elevation of right ventricular pressure increases the early systolic backflow, largely prevents mid-systolic forward flow, and accentuates early diastolic flow. It is suggested that this pattern does not represent that in arterioles in deep layers of the myocardium.
In other experiments the septal artery was perfused through an orifice meter at variable pressures to determine the pressure required to negate mid-systolic flow at high right ventricular pressures. The results indicate that pressures considerably above aortic or right ventricular systolic pressures are required to generate forward mid-systolic septal flow.
The mean septal flow was quantitated in terms of total common left inflow. It was found that an average of 16.0% of common left flow enters the septal artery. The significance of this has been discussed in terms of its relationship to the venous drainage of common left coronary arterial inflow.