bluuebunny/crossref_metadata_2025_split huggingface dataset:
Role of endothelium-derived nitric oxide in the abnormal endothelium-dependent vascular relaxation of patients with essential hypertension.
Authors: Panza J A , Casino P R , Kilcoyne C M , Quyyumi A A 
Published: June 2012

BACKGROUND
Patients with essential hypertension have abnormal endothelium-dependent vasodilation. Because the endothelium exerts its action on the vascular smooth muscle through the release of several substances, it is important to identify which of these factors is involved in the abnormal response of hypertensive arteries.

METHODS AND RESULTS
To investigate the role of endothelium-derived nitric oxide in this abnormality, we studied the vascular effect of the arginine analogue NG-monomethyl-L-arginine, an inhibitor of the endothelial synthesis of nitric oxide, under baseline conditions and during infusion of acetylcholine, an endothelium-dependent vasodilator, and sodium nitroprusside, a direct smooth muscle dilator. The study included 11 hypertensive patients (seven men; age, 46.5 +/- 9 years) and 10 normal control subjects (seven men; age, 45.7 +/- 7 years). Drugs were infused into the brachial artery, and the response of the forearm vasculature was measured by strain-gauge plethysmography. Basal blood flow was similar in normal control subjects and hypertensive patients (2.97 +/- 0.7 versus 2.86 +/- 1.1 mL.min-1.100 mL-1, respectively). NG-monomethyl-L-arginine produced a significantly greater decrease in blood flow in control subjects than in patients (1.08 +/- 0.6 versus 0.32 +/- 0.4 mL.min-1.100 mL-1; p < 0.004). The vasodilator response to acetylcholine was reduced in patients compared with control subjects (maximum flow, 8.2 +/- 4 versus 16.4 +/- 8 mL.min-1.100 mL-1; p < 0.001). NG-monomethyl-L-arginine blunted the vasodilator response to acetylcholine in control subjects (maximum flow decreased from 16.4 +/- 8 to 7.01 +/- 3 mL.min-1.100 mL-1; p < 0.004); however, the arginine analogue did not significantly alter the response to acetylcholine in hypertensive patients (maximum flow, 8.2 +/- 4 versus 8.01 +/- 5 mL.min-1.100 mL-1). NG-monomethyl-L-arginine did not modify the vasodilator response to sodium nitroprusside in either control subjects or patients.

CONCLUSIONS
These findings indicate that patients with essential hypertension have a defect in the endothelium-derived nitric oxide system that may at least partly account for both the increased vascular resistance under basal conditions and the impaired response to endothelium-dependent vasodilators.
Aspirin versus coumadin in the prevention of reocclusion and recurrent ischemia after successful thrombolysis: a prospective placebo-controlled angiographic study. Results of the APRICOT Study.
Authors: Meijer A , Verheugt F W , Werter C J , Lie K I , van der Pol J M , van Eenige M J 
Published: June 2012

BACKGROUND
Successful coronary thrombolysis involves a risk for reocclusion that cannot be prevented by invasive strategies. Therefore, we studied the effects of three antithrombotic regimens on the angiographic and clinical courses after successful thrombolysis.

METHODS AND RESULTS
Patients treated with intravenous thrombolytic therapy followed by intravenous heparin were eligible when a patent infarct-related artery was demonstrated at angiography < 48 hours. Three hundred patients were randomized to either 325 mg aspirin daily or placebo with discontinuation of heparin or to Coumadin with continuation of heparin until oral anticoagulation was established (international normalized ratio, 2.8-4.0). After 3 months, in which conservative treatment was intended, vessel patency and ventricular function were reassessed in 248 patients. Reocclusion rates were not significantly different: 25% (23 of 93) with aspirin, 30% (24 of 81) with Coumadin, and 32% (24 of 74) with placebo. Reinfarction was seen in 3% of patients on aspirin, in 8% on Coumadin, and in 11% on placebo (aspirin versus placebo, p < 0.025; other comparison, p = NS). Revascularization rate was 6% with aspirin, 13% with Coumadin, and 16% with placebo (aspirin versus placebo, p < 0.05; other comparisons, p = NS). Mortality was 2% and did not differ between groups. An event-free clinical course was seen in 93% with aspirin, in 82% with Coumadin, and in 76% with placebo (aspirin versus placebo, p < 0.001; aspirin versus Coumadin, p < 0.05). An event-free course without reocclusion was observed in 73% with aspirin, in 63% with Coumadin, and in 59% with placebo (p = NS). An increase of left ventricular ejection fraction was only found in the aspirin group (4.6%, p < 0.001).

CONCLUSIONS
At 3 months after successful thrombolysis, reocclusion occurred in about 30% of patients, regardless of the use of antithrombotics. Compared with placebo, aspirin significantly reduces reinfarction rate and revascularization rate, improves event-free survival, and better preserves left ventricular function. The efficacy of Coumadin on these end points appears less than that of aspirin. The still-high reocclusion rate emphasizes the need for better antithrombotic therapy in these patients.
Ultrasound-assisted cannulation of the internal jugular vein. A prospective comparison to the external landmark-guided technique.
Authors: Denys B G , Uretsky B F , Reddy P S 
Published: June 2012

BACKGROUND
Central venous access is an essential part of patient management in many clinical settings and is usually achieved with a blinded, external landmark-guided technique. The purpose of this study is to evaluate whether an ultrasound technique can improve on the traditional method.

METHODS AND RESULTS
We prospectively evaluated an ultrasound-guided method in 302 patients undergoing internal jugular venous cannulation and compared the results with 302 patients in whom an external landmark-guided technique was used. Ultrasound was used exclusively in an additional 626 patients. Cannulation of the internal jugular vein was achieved in all patients (100%) using ultrasound and in 266 patients (88.1%) using the landmark-guided technique (p < 0.001). The vein was entered on the first attempt in 78% of patients using ultrasound and in 38% using the landmark technique (p < 0.001). Average access time (skin to vein) was 9.8 seconds (2-68 seconds) by the ultrasound approach and 44.5 seconds (2-1,000 seconds) by the landmark approach (p < 0.001). Using ultrasound, puncture of the carotid artery occurred in 1.7% of patients, brachial plexus irritation in 0.4%, and hematoma in 0.2%. In the external landmark group, puncture of the carotid artery occurred in 8.3% of patients (p < 0.001), brachial plexus irritation in 1.7% (p < 0.001), and hematoma in 3.3% (p < 0.001).

CONCLUSIONS
Ultrasound-guided cannulation of the internal jugular vein significantly improves success rate, decreases access time, and reduces complication rate. These results suggest that this technique may be preferred in complicated cases or when access problems are anticipated.
Regional myocardial blood flow and glucose utilization in symptomatic patients with hypertrophic cardiomyopathy.
Authors: Nienaber C A , Gambhir S S , Mody F V , Ratib O , Huang S C , Phelps M E , Schelbert H R 
Published: June 2012

BACKGROUND
Previous studies suggested the presence of myocardial ischemia in symptomatic patients with hypertrophic cardiomyopathy. Positron emission tomography, a technique that can identify metabolic consequences of ischemia in coronary artery disease, permits the noninvasive measurements of regional myocardial blood flow and glucose metabolism. This new quantitative imaging approach should therefore be suitable for detecting a possible enhancement of glucose utilization in myocardium of patients with hypertrophic cardiomyopathy and thus may help to elucidate the pathomechanism of ischemia in this disease.

METHODS AND RESULTS
In 13 symptomatic patients with hypertrophic cardiomyopathy, myocardial blood flow and glucose utilization were measured with intravenous N-13-ammonia and F-18 deoxyglucose at rest and, in four patients, again during supine bicycle exercise. At rest, blood flow was significantly lower in hypertrophied than in normal myocardium (0.78 +/- 0.19 versus 0.99 +/- 0.13 mL.min-1.g-1, p < 0.025), whereas rates of glucose utilization were similar (0.88 +/- 0.31 versus 0.87 +/- 0.35 mumol.min-1.g-1). With exercise, blood flow and glucose utilization failed to increase in hypertrophic and normal segments but became more heterogeneously distributed throughout the left ventricular myocardium. Blood flow-metabolism mismatches indicative of myocardial ischemia were noted in three patients at rest and in three of the four patients during exercise and were due to reduced flow in the presence of maintained glucose uptake. The discordance between flow and glucose metabolism in hypertrophied myocardium was significantly more prominent in younger than in older patients.

CONCLUSIONS
Normal or even elevated rates of glucose utilization and the presence of diminished blood flow in hypertrophied relative to normal myocardium suggest the presence of myocardial ischemia in symptomatic hypertrophic cardiomyopathy. The age dependence of blood flow metabolism disparity suggests differences in the underlying pathophysiology or severity of disease.
Quantitative planar rest-redistribution 201Tl imaging in detection of myocardial viability and prediction of improvement in left ventricular function after coronary bypass surgery in patients with severely depressed left ventricular function.
Authors: Ragosta M , Beller G A , Watson D D , Kaul S , Gimple L W 
Published: June 2012

BACKGROUND
Although many patients with multivessel coronary artery disease (CAD) and severely depressed left ventricular (LV) function will benefit from coronary artery bypass graft surgery (CABG), surgeons may be reluctant to perform CABG on these patients without evidence of myocardial viability in regions of severe asynergy. We hypothesized that quantitative planar rest-redistribution 201Tl imaging would identify viable myocardium and predict improved regional and global function after revascularization in patients with depressed LV function and CAD.

METHODS AND RESULTS
Twenty-one patients (mean LV ejection fraction, 0.27 +/- 0.05) were studied. Regional and global LV functions were evaluated before and 8 weeks after CABG with radionuclide ventriculography. Segments were prospectively classified as showing normal, mildly reduced, or severely reduced viability on the basis of quantitative analysis of defect severity and redistribution on planar resting 201Tl imaging. By 201Tl criteria, 90% of hypokinetic segments were classified with normal or mildly reduced viability. Among akinetic or dyskinetic segments, 20% had normal 201Tl uptake, 53% had mildly reduced viability, and only 27% had severely reduced viability. 201Tl viability criteria identified segments that improved function after CABG. Sixty-two percent of severely asynergic segments with normal viability and 54% with mildly reduced viability improved function after surgery, but only 23% with severely reduced viability improved function (p = 0.002). When only adequately revascularized segments were considered, the predictive value of a positive preoperative viability scan for functional improvement was 73%. The greatest improvement in global LV function after CABG occurred in patients with the greatest number of asynergic segments classified as viable before surgery (p < 0.01). In 10 patients with more than seven viable, asynergic segments, mean LV ejection fraction increased significantly after CABG (0.29 +/- 0.07 to 0.41 +/- 0.11, p = 0.002). In 11 patients with seven or fewer viable, asynergic segments, mean LV ejection fraction remained unchanged after revascularization (0.27 +/- 0.05 to 0.30 +/- 0.08, p = NS).

CONCLUSIONS
In patients with CAD and severely depressed LV function, preoperative quantitative planar rest-redistribution. 201Tl imaging identifies viability in many asynergic myocardial segments, and these segments frequently improve function after CABG. The presence of numerous asynergic but viable myocardial segments before surgery correlated significantly with improvement in global LV function after bypass surgery.
TIMI perfusion grade 3 but not grade 2 results in improved outcome after thrombolysis for myocardial infarction. Ventriculographic, enzymatic, and electrocardiographic evidence from the TEAM-3 Study.
Authors: Anderson J L , Karagounis L A , Becker L C , Sorensen S G , Menlove R L 
Published: June 2012

BACKGROUND
Coronary patency has been used as a measure of thrombolysis success after acute myocardial infarction. The Thrombolysis in Myocardial Infarction (TIMI) Study Group perfusion grades have gained wide acceptance, with grades 0 (no distal flow) and 1 perfusion (minimal flow) being designated as thrombolysis failures and grades 2 (partial perfusion) and 3 (complete perfusion) as thrombolysis successes. However, the significance of the individual TIMI grades on clinical outcome has not been adequately assessed.

METHODS AND RESULTS
To evaluate the functional significance of TIMI perfusion grades, we compared 1-day coronary patency status with ventriculographic, enzymatic, and ECG indexes of acute myocardial infarction in 298 patients treated with anistreplase or alteplase within 4 hours of myocardial infarction symptom onset. Radionuclide ejection fraction was determined at 1 week and at 1 month. Perfusion grades for the entire study population were distributed as 12% (n = 37) grades 0/1, 13% (n = 40) grade 2, and 74% (n = 221) grade 3. Patency profile did not differ between the two thrombolytic regimens. Further coronary interventions were performed after the 1-day patency determination in 43% of patients (43%, 48%, 42%, respectively, in grades 0/1, 2, and 3 patients). The outcome of grade 2 patients did not differ from grades 0/1 patients in ejection fraction, enzyme peaks, ECG markers, or morbidity index. In contrast, grade 3 patients, compared with grades 0-2 patients, showed 1) a greater global ejection fraction at 1 week (54% versus 49%, p = 0.006) and at 1 month (54% versus 49%, p = 0.01), 2) a greater infarct zone ejection fraction at 1 week (41% versus 33%, p = 0.003) and at 1 month (42% versus 32%, p = 0.003), 3) smaller enzyme peaks, significant for lactate dehydrogenase, and shorter times to enzyme peaks, significant for all four enzymes, 4) a smaller QRS score at discharge and at 1 month, and 5) a trend toward a lower morbidity index.

CONCLUSIONS
Grade 3 flow predicts significantly better outcomes than lesser grades of flow and represents an important measure of reperfusion success.
Comparison of coronary angiographic findings in acute and chronic first presentation of ischemic heart disease.
Authors: Bogaty P , Brecker S J , White S E , Stevenson R N , el-Tamimi H , Balcon R , Maseri A 
Published: June 2012

BACKGROUND
It is generally assumed that the clinical manifestations of ischemic heart disease occur randomly on the same underlying pathological process. Therefore, coronary angiographic findings should be similar whether the first presentation of ischemic heart disease is acute myocardial infarction or uncomplicated chronic stable angina.

METHODS AND RESULTS
We studied 102 patients (men < or = 60 years old, women < or = 65 years old) presenting with either acute myocardial infarction as first manifestation of coronary artery disease with a concomitant coronary angiogram (55 patients; mean age, 50.2 years) or stable angina for at least 2 years with no history, ECG, or left ventriculographic evidence of any acute event and with an angiogram performed at least 2 years after initial symptoms (47 patients; mean age at symptom onset, 51.7 years). These angiograms were evaluated blindly for severity (number of vessels diseased, stenoses > or = 50%, occlusions), extent of disease (with an index derived by assigning a score of 0-3 per segment, depending on the proportion of lumen length irregularity and dividing the sum by the number of visualized segments), and pattern (discrete: three or fewer loci of disease never involving more than 50% of the length of any segment or diffuse: anything exceeding this). Patients with unheralded myocardial infarction had fewer vessels diseased, fewer stenoses and occlusion, and a lower extent index than those with uncomplicated stable angina (mean +/- SD of 1.3 +/- 0.8 versus 2.1 +/- 0.8, p < 0.001; 2.1 +/- 1.8 versus 3.9 +/- 1.8, p < 0.001; 0.6 +/- 0.6 versus 1.0 +/- 0.9, p < 0.02; and 0.6 +/- 0.5 versus 1.2 +/- 0.5, p < 0.001, respectively). A discrete pattern was present in 54.5% of patients with unheralded infarction and in only 8.5% of those with uncomplicated angina (p < 0.001).

CONCLUSIONS
These very different angiographic findings suggest that unheralded acute myocardial infarction and uncomplicated chronic stable angina do not occur randomly on a common atherosclerotic background but rather that additional factors, such as a varying propensity to thrombosis, may predispose to one or the other of these two clinical syndromes.
Risk of stroke in adults with cyanotic congenital heart disease.
Authors: Perloff J K , Marelli A J , Miner P D 
Published: June 2012

BACKGROUND
Adults with cyanotic congenital heart disease and elevated hematocrit levels are often phlebotomized because of an assumed risk of cerebral arterial thrombotic stroke. Whether a relation exists between hematocrit level, symptomatic erythrocytosis (hyperviscosity), and stroke remains to be established in this patient population.

METHODS AND RESULTS
Accordingly, 112 cyanotic patients 19-74 years old (mean, 36 +/- 11.7 years) in the UCLA Adult Congenital Heart Disease Center Registry were selected for study by virtue of continuous observation for 1-12 years (total, 748 patient-years). Patients with independent risk factors for embolic or vasospastic stroke were excluded. The study patients were then divided into two groups: 1) compensated erythrocytosis (stable hematocrit levels of 46.0-72.7% [mean, 57.5 +/- 7.2%], iron replete, absent or mild hyperviscosity symptoms), and 2) decompensated erythrocytosis (unstable rising hematocrit levels of 61.5-75.0% [mean, 69.5 +/- 10.6%], iron deficiency, marked-to-severe hyperviscosity symptoms). No patient with either compensated or decompensated erythrocytosis, irrespective of hematocrit level, iron stores, or the presence, degree, or recurrence of cerebral hyperviscosity symptoms, progressed to clinical evidence of a complete stroke (cerebral arterial thrombosis with brain infarction).

CONCLUSIONS
Because a risk of stroke caused by cerebral arterial thrombosis was not demonstrated, because the circulatory effects of phlebotomy are transient, and because of the untoward sequelae of phlebotomy-induced iron deficiency, we recommend phlebotomy for the temporary relief of significant, intrusive hyperviscosity symptoms but not for the hematocrit level per se. According to our data, phlebotomy is not warranted to reduce an assumed risk of stroke because that risk did not materialize.
Stimulation of plasminogen activator inhibitor in vivo by infusion of angiotensin II. Evidence of a potential interaction between the renin-angiotensin system and fibrinolytic function.
Authors: Ridker P M , Gaboury C L , Conlin P R , Seely E W , Williams G H , Vaughan D E 
Published: June 2012

BACKGROUND
Recent clinical trial data indicate that the use of angiotensin converting enzyme (ACE) inhibitors among patients with left ventricular dysfunction results in reduced rates of coronary thrombosis, a provocative finding that suggests a potential interaction between the renin-angiotensin system and fibrinolytic function.

METHODS AND RESULTS
In four normotensive subjects and six hypertensive patients, we investigated whether infusion of angiotensin II (Ang II) affected circulating levels of plasminogen activator inhibitor-1 (PAI-1), the most important physiological inhibitor of tissue-type plasminogen activator (t-PA). Overall, mean levels of PAI-1 antigen increased significantly from 20.1 ng/mL before Ang II infusion to 36.0 ng/mL at the end of Ang II infusion (p = 0.008), whereas no change in PAI-1 was observed for control subjects infused with 5% dextrose (p = 0.46). Among the normotensive subjects for whom graded doses of Ang II were infused at 0, 1, 3, and 10 ng.kg-1.min-1, mean PAI-1 levels increased sequentially from 14.7 ng/mL to 23.0, 26.8, and 33.5 ng/mL, a dose-response relation that, compared with controls, was highly significant (p < 0.001). Among the hypertensive patients for whom a single 45-minute infusion of Ang II was given at a dose of 3 ng.kg-1.min-1, PAI-1 levels increased from 23.7 to 37.7 ng/mL, whereas PAI-1 levels among control subjects infused with 5% dextrose decreased from 16.9 to 10.8 ng/mL (p = 0.04). Finally, when compared with infusion of 5% dextrose solution, infusion of Ang II appeared to have little effect on circulating levels of t-PA antigen.

CONCLUSIONS
These in vivo data suggest that infusion of Ang II results in a rapid increase in circulating levels of PAI-1, a finding that may help to explain clinical observations linking the renin-angiotensin system and thrombotic risk.
Cardiorenal and neurohumoral function in a canine model of early left ventricular dysfunction.
Authors: Redfield M M , Aarhus L L , Wright R S , Burnett J C 
Published: June 2012

BACKGROUND
Recent studies have reported that asymptomatic left ventricular dysfunction (ALVD) in humans is characterized by early neurohumoral activation. Specifically, atrial natriuretic factor (ANF) and norepinephrine are activated without activation of the renin-angiotensin-aldosterone system (RAAS). The current study describes hemodynamic and renal function associated with this neurohumoral profile in a canine model of early and presumably "asymptomatic" ventricular dysfunction. We hypothesized that the neurohumoral profile observed in ALVD is associated with preservation of renal function despite significant hemodynamic compromise.

METHODS AND RESULTS
ALVD was produced by ventricular pacing at 180 beats per minute for 10 days. Intravascular volume expansion was performed before and after producing ALVD in eight conscious dogs. The model of ALVD was characterized by decreases in ejection fraction (48 +/- 2 to 29 +/- 4%), cardiac output (4.64 +/- 0.29 to 2.89 +/- 0.17 L/min), and mean arterial pressure (119 +/- 4 to 108 +/- 4 mm Hg). Atrial pressures and systemic vascular resistance were increased. ANF (60 +/- 19 to 165 +/- 27 pg/mL) and norepinephrine (382 +/- 127 to 690 +/- 211 pg/mL) were activated, whereas the RAAS was not. Creatinine clearance and sodium excretion (UNa V) were unchanged after producing ALVD. The natriuretic response to volume expansion in ALVD was completely intact, with increases in UNa V similar to that observed with volume expansion in ALVD was completely intact, with increases in UNa V similar to that observed with volume expansion before producing ALVD.

CONCLUSIONS
The current study demonstrates that significant ventricular dysfunction with peripheral vasoconstriction can be associated with normal renal function and thus suggests an important functional role for the neurohumoral profile of ALVD in preserving sodium balance.