bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hypertension and left ventricular hypertrophy are associated with impaired endothelium-mediated relaxation in human coronary resistance vessels.
Authors: Treasure C B , Klein J L , Vita J A , Manoukian S V , Renwick G H , Selwyn A P , Ganz P , Alexander R W 
Published: June 2012

BACKGROUND
Patients with hypertension and myocardial hypertrophy may have signs and symptoms of myocardial ischemia in the absence of obstructive coronary disease. Prior investigations have demonstrated impaired coronary flow reserve and have led to speculation that microvascular dysfunction might contribute to ischemia in these patients. Experimental studies have shown that the endothelium, an important regulator of microvascular tone, can be damaged by hypertension and is dysfunctional in cardiomyopathy. We hypothesized that endothelium-dependent vasodilation is impaired in the coronary microvasculature of patients with hypertension and ventricular hypertrophy.

METHODS AND RESULTS
We studied coronary microvascular responses in 10 patients with left ventricular hypertrophy secondary to essential hypertension (HTN) (mean arterial pressure at catheterization, 151/94 mm Hg; mean posterior wall thickness, 1.4 +/- 0.1 cm) and nine normal control subjects with no history of hypertension (mean arterial pressure at catheterization, 128/75 mm Hg; mean posterior wall thickness, 1.0 +/- 0.02 cm) using the intracoronary Doppler catheter and quantitative angiography to assess changes in coronary blood flow (CBF). All patients had normal left ventricular systolic function. To assess microvascular endothelial function, we infused the endothelium-dependent vasodilator acetylcholine (10(-8)-10(-6) M) and the endothelium-independent vasodilator adenosine (10(-6)-10(-4) M) into the left anterior descending coronary artery. In response to acetylcholine, CBF increased only 32 +/- 25% in HTN patients, whereas CBF increased 192 +/- 39% in normal control subjects (p = 0.003). CBF increased 465 +/- 93% in HTN patients and 439 +/- 41% in normal control subjects in response to adenosine (p = NS). The proportion of coronary flow reserve attributable to endothelium-dependent dilation (obtained from peak acetylcholine/peak adenosine flow response) was 48 +/- 9% in normal control subjects but only 7 +/- 8% in HTN patients (p = 0.008).

CONCLUSIONS
Endothelium-dependent vasodilation is markedly impaired in the coronary microvessels of patients with hypertension and ventricular hypertrophy. Loss of this vasodilator mechanism may contribute to disordered coronary flow regulation and the ischemic manifestations of hypertensive heart disease.
Residual coronary reserve despite decreased resting blood flow in patients with critical coronary lesions. A study by technetium-99m human albumin microsphere myocardial scintigraphy.
Authors: Parodi O , Sambuceti G , Roghi A , Testa R , Inglese E , Pirelli S , Spinelli F , Campolo L , L'Abbate A 
Published: June 2012

BACKGROUND
Experimental data demonstrate the persistence of a transmural vasodilator reserve in the face of depressed resting myocardial perfusion. The present study was designed to determine whether resting myocardial hypoperfusion indicates exhausted coronary reserve (CR).

METHODS AND RESULTS
Fifteen patients with stable angina, isolated left anterior descending coronary artery (LAD) stenosis, and no previous myocardial infarction were evaluated by means of 99mTc human albumin microsphere scintigraphy. Regional myocardial perfusion and CR were assessed at baseline and after LAD papaverine (10-12 mg) by means of two microsphere injections in the left ventricle and compared with five normal subjects. Two 300-second scans were obtained with a mobile gamma camera positioned in the 70 degrees left anterior oblique projection; actual microsphere distribution after papaverine was obtained by image subtraction. The two arterial input functions (basal and papaverine) were measured from the first-pass time-activity curves and validated with the reference arterial sample technique. From the comparison of circumferential profile analysis between patients and normal subjects, nine patients (group 1A) showed perfusion defects at rest (reduction of percent radioactivity below 2 SD of normal subjects) in the LAD territory, and the other six (group 1B) showed homogeneous perfusion. CR (papaverine/resting perfusion) was 3.8 +/- 0.2 and 1.51 +/- 0.27 in normal subjects and in ischemic patients, respectively (p < 0.01). Despite resting hypoperfusion, group 1A showed a papaverine-recruitable CR similar to that of group 1B (1.57 +/- 0.33 and 1.43 +/- 0.16, respectively, p = NS).

CONCLUSIONS
In patients with stable angina pectoris, isolated LAD stenosis, and no previous myocardial infarction, microsphere scintigraphy disclosed a high incidence of resting perfusion defects; in those patients, a residual CR was observed despite decreased resting blood flow.
Characterization of double potentials during ventricular tachycardia. Studies during transient entrainment.
Authors: Olshansky B , Moreira D , Waldo A L 
Published: June 2012

BACKGROUND
Double potentials have been recorded during reentrant tachycardias in animal models. Although they have also been recorded during ventricular tachycardia in humans, their meaning is uncertain.

METHODS AND RESULTS
We used transient entrainment as a method to help further understand the meaning of double potentials recorded during ventricular tachycardia in humans. Three patients with ventricular tachycardia (cycle lengths, 500, 450, and 290 msec) were studied. During transient entrainment of ventricular tachycardia (pacing cycle length, 470-260 msec), both double potential deflections were captured at the pacing cycle length. One deflection was captured with a short activation time, and the other deflection was captured with a long activation time. During ventricular pacing, the deflections were associated by the long rather than the short interdeflection interval. At termination of pacing, each double potential deflection was associated with separate but sequential QRS complexes, and each deflection maintained the same electrogram morphology at relatively "slow" overdrive pacing rates. The short interdeflection interval shortened further with faster pacing rates (to less than the ventricular refractory period), making it unlikely that both deflections of the double potential represent active depolarization of the same tissue. In two patients, at a critically rapid pacing rate, one of the double potential deflections changed morphology abruptly, associated with a shortened stimulus-to-double potential time interval (from 520 to 110 msec and from 530 to 240 msec, respectively), indicating a change in the direction of activation that caused that deflection. Interruption of ventricular tachycardia was associated with disappearance of the double potentials at the same recording site. The double potentials did not immediately bracket an area of slow conduction.

CONCLUSIONS
These data suggest that double potentials recorded only during ventricular tachycardia represent activation wave fronts on either side of an area of block within a reentrant circuit. Thus, double potentials recorded during ventricular tachycardia in these patients do not appear to represent slow conduction per se but rather appear to represent an area of block at the center of a reentrant circuit around which the reentrant wave front circulates.
Effect of subcutaneous sumatriptan, a selective 5HT1 agonist, on the systemic, pulmonary, and coronary circulation.
Authors: MacIntyre P D , Bhargava B , Hogg K J , Gemmill J D , Hillis W S 
Published: June 2012

BACKGROUND
Sumatriptan (GR43175) is a selective 5-hydroxytryptamine (5HT1) receptor agonist effective in the acute treatment of migraine. Recent in vitro experiments suggest that it has vasoactive properties in vascular beds distinct from the cerebral circulation. The object of this study was to assess the vasoactive effects of the standard 6-mg subcutaneous dose of sumatriptan used in migraine on the systemic and pulmonary circulations and the coronary artery vasculature.

METHODS AND RESULTS
Ten patients undergoing diagnostic coronary arteriography were studied with digital subtraction angiography and invasive hemodynamic monitoring. After subcutaneous injection of sumatriptan, there was no significant change in heart rate or ECG morphology. There was a significant rise in the systemic (20%, p < 0.05 by ANOVA) and pulmonary artery (40%, p < 0.05 by ANOVA) pressures. There was no change in cardiac output, but there was a significant increase in total systemic (27%, p < 0.05) and total pulmonary vascular resistance (40%, p < 0.05). Sumatriptan caused a significant reduction (p < 0.001 by ANOVA) in mean absolute coronary artery diameter, from 4.36 +/- 1.60 mm at baseline to 3.67 +/- 1.49 mm (16%) at 10 minutes and to 3.63 +/- 1.49 mm (17%) at 30 minutes after injection. There were no clinical sequelae.

CONCLUSIONS
Sumatriptan, a 5HT1 receptor agonist administered by the subcutaneous route, causes a vasopressor response in the systemic and pulmonary arterial circulations and coronary artery vasoconstriction.
Tricuspid atresia presenting in infancy. Survival and suitability for the Fontan operation.
Authors: Franklin R C , Spiegelhalter D J , Sullivan I D , Anderson R H , Thoele D G , Shinebourne E A , Deanfield J E 
Published: June 2012

BACKGROUND
The Fontan operation is the usual goal of therapy for children with tricuspid atresia. The influences of morphology and different management strategies on survival and subsequent suitability for this procedure are crucial but unstudied in an unselected population during the Fontan era.

METHODS AND RESULTS
The fates of 237 consecutive infants with tricuspid atresia were reviewed (1972-1987; median follow-up, 8.0 years). Overall actuarial survival was 72% at 1 year, 53% at 5 years, and 46% at 10 years. Univariate risk factor analysis established that discordant ventriculoarterial connections (24% of the group; relative risk, 2.7), pulmonary atresia (14%, 2.3), aortic arch obstruction (7%, 2.9), and subaortic stenosis (8%, 4.2) were associated with poor survival, whereas pulmonary stenosis (60%, 0.52), balanced pulmonary blood flow (9%, 0.25), and older age at presentation (33%, 0.42) were beneficial. Multivariate analysis allowed the creation of predictive patient-specific survival curves and two additive indexes. Survival was worse for patients who underwent banding of the pulmonary trunk with aortic arch repair than for other individual palliative procedures (p < 0.001). On retrospective review, 204 patients (86%) were judged suitable for a future Fontan procedure at presentation. However, 99 (48%) of these are known to have died before a Fontan operation or became unsuitable for such surgery during follow-up, mostly because of death after palliative surgery (23 patients, 11%), sudden death (18 patients, 9%), and new adverse features (32 patients, 16%) such as subaortic stenosis, pulmonary arterial distortion, and ventricular dysfunction.

CONCLUSIONS
Management in infancy must aim to ensure survival and maintain suitability for a Fontan-type operation. The accumulating incidence of adverse events with increasing age would argue in favor of undertaking definitive surgery in early childhood in most patients.
Effect of aspirin on coronary collateral blood flow.
Authors: Altman J D , Dulas D , Pavek T , Bache R J 
Published: June 2012

BACKGROUND
Although aspirin exerts beneficial antiplatelet activity in patients with coronary artery disease, cyclooxygenase blockade produced by aspirin causes a potentially deleterious effect by interrupting endothelial production of prostacyclin. Collateral vessels that develop in response to coronary occlusion display prominent endothelial cell proliferation and undergo vasoconstriction in response to indomethacin. This study was performed to test the hypothesis that cyclooxygenase blockade with aspirin would cause constriction of coronary collateral vessels and that such vasoconstriction would be reversed with nitroglycerin.

METHODS AND RESULTS
Collateral vessel growth was induced by embolic occlusion of the left anterior descending coronary artery in dogs. Four to 6 months later, coronary collateral flow was measured as retrograde flow from the cannulated collateral-dependent artery. Aspirin (1 mg/kg i.v.) caused 70 +/- 8% blockade of the increase in coronary blood flow produced by intra-arterial arachidonic acid and decreased retrograde flow from 37 +/- 7 to 28 +/- 7 ml/min (p < 0.03). Increasing the dose of aspirin to 15 mg/kg i.v. caused 91 +/- 3% blockade of the response to arachidonic acid and further decreased retrograde flow to 21 +/- 4 ml/min (p < 0.01). After aspirin administration, nitroglycerin (150 micrograms/min i.c.) reversed the collateral constriction and increased retrograde flow to 37 +/- 10 ml/min (p < 0.01).

CONCLUSIONS
These data suggest that products of cyclooxygenase metabolism cause tonic vasodilation of well-developed coronary collateral vessels. Blockade of cyclooxygenase with even low-dose aspirin caused collateral vessel constriction with a decrease in collateral blood flow. However, nitroglycerin was able to fully reverse aspirin-induced collateral vasoconstriction and restore flow to the control level.
Signal-averaged electrocardiogram. Improved identification of patients with ventricular tachycardia using a 28-lead optimal array.
Authors: Ho D S , Denniss R A , Uther J B , Ross D L , Richards D A 
Published: June 2012

BACKGROUND
Although the signal-averaged ECG (SAECG) is currently the best noninvasive test to identify patients with ventricular tachycardia (VT) following myocardial infarction (MI), it is still a relatively insensitive test. Body surface mapping has improved the sensitivity of ECG in detecting various cardiac diseases. This study applied body surface mapping to the SAECG in the form of a clinically practical, 28-lead optimal array and compared its sensitivity and specificity with those of an orthogonal array.

METHODS AND RESULTS
Two hundred twenty-three patients with previous MI (82 with inducible VT) underwent SAECG using 28 surface electrodes from which were obtained a three-lead orthogonal array and a 28-lead optimal array (optimal). From the orthogonal array, two QRS durations (QRSd) were obtained using the combined vector magnitude method (CVM) and the earliest onset to latest offset of the three individually filtered leads (individual). From the optimal array, 28 QRSd were obtained, each defined as the duration from the earliest onset of any of the 28 leads to the offset of each individually filtered lead. QRSd > 120 msec in > or = 3 leads was considered abnormal. For CVM and individual, QRSd of > 120 msec were considered abnormal. While the specificity of each method was comparable (84%, 86%, and 84% for CVM, individual, and optimal, respectively), the sensitivity of optimal (70%) was significantly greater than the sensitivity of CVM (54%) (p = 0.001) or individual (59%) (p = 0.004). The magnitude of improvement in sensitivity, 16% and 15%, respectively, was equal for anterior (n = 120) and inferior (n = 103) infarctions.

CONCLUSIONS
Body surface mapping using the 28-lead optimal array significantly improved the sensitivity of the SAECG without loss of specificity. The increased sensitivity was of equal magnitude for inferior and anterior infarctions. The superiority and practicality of the 28-lead optimal array make it worth pursuing as an option for further refinement in SAECG:
Superoxide dismutase restores contractile and metabolic dysfunction through augmentation of adenosine release in coronary microembolization.
Authors: Takashima S , Hori M , Kitakaze M , Sato H , Inoue M , Kamada T 
Published: June 2012

BACKGROUND
This study was undertaken to test the hypothesis that administration of superoxide dismutase (SOD) restores the contractile and metabolic dysfunction in coronary microembolization and that these beneficial effects of SOD are attributable to the restoration of 5'-nucleotidase activity and subsequent augmentation of adenosine release.

METHODS AND RESULTS
In 78 dogs before and after an injection of microspheres (15 microns in diameter) into the left anterior descending coronary artery, regional coronary blood flow (CBF), fractional shortening (FS), and lactate extraction ratio (LER) were measured with and without administration of recombinant human SOD (50 micrograms/kg/min i.c.). In the untreated dogs (n = 6), both FS and LER decreased after coronary microembolization (2.0 x 10(5) microspheres per ml CBF [mL/min]). FS and LER decreased from 24.2 +/- 1.3% to 5.1 +/- 1.2% and from 23.0 +/- 1.1% to -10.5 +/- 2.9%, respectively. These ischemic changes were associated with coronary hyperemic flow (141 +/- 8 versus 92 +/- 1 mL/100 g/min) and adenosine release (5.8 +/- 0.5 versus 0.4 +/- 0.1 nmol/100 g/min). Pretreatment with SOD augmented the hyperemic flow to 164 +/- 4 mL/100 g/min and enhanced the release of adenosine (9.6 +/- 0.6 nmol/100 g/min) associated with improvement of functional and metabolic dysfunction (FS, 14.8 +/- 2.3%; LER, 15.1 +/- 3.1%). Administration of SOD at 10 minutes (n = 5) and 30 minutes (n = 5) after coronary embolization restored the contractile function and lactate metabolism (at 10 minutes: FS, 16.7 +/- 2.2% and LER, 16.7 +/- 3.9%; at 30 minutes: FS, 11.1 +/- 1.3% and LER, 7.2 +/- 3.1%). However, administration of SOD 60 minutes after coronary embolization (n = 6) did not restore the contractile and metabolic dysfunction. The restoration of the contractile and metabolic dysfunction by SOD treatment was blunted by adenosine receptor blockade with 8-phenyltheophylline (n = 5). Myocardial 5'-nucleotidase activity at 2 hours after embolization was restored with SOD treatment at 10 minutes (n = 5) and 30 minutes (n = 5) after embolization. However, SOD treatment at 60 minutes after embolization (n = 6) did not restore 5'-nucleotidase activity compared with the SOD pretreatment group. Furthermore, coronary submaximal vasodilation induced by papaverine (n = 5) and adenosine (n = 5) abolished the beneficial effects of SOD.

CONCLUSIONS
We conclude that 1) in sustained myocardial ischemia, SOD treatment attenuates ischemic injury caused by coronary microembolization by restoration of 5'-nucleotidase activity and augmentation of adenosine release; 2) this beneficial effect of SOD is observed even after coronary microembolization; and 3) the beneficial effects of SOD are attributable to coronary vasodilation produced by augmented adenosine release.
Magnetic resonance jet velocity mapping in mitral and aortic valve stenosis.
Authors: Kilner P J , Manzara C C , Mohiaddin R H , Pennell D J , Sutton M G , Firmin D N , Underwood S R , Longmore D B 
Published: June 2012

BACKGROUND
Magnetic resonance (MR) phase-shift velocity mapping is an established method for measurement of nonturbulent intravascular flow. Shortening the echo time of the MR sequence to 3.6 msec allowed application of the technique to turbulent jet flow. The objective of this study was validation of MR jet velocity mapping in patients with cardiac valve stenosis.

METHODS AND RESULTS
We used a 0.5-T Picker MR machine to measure peak poststenotic jet velocity in 15 consecutive patients recruited with known valve disease (six mitral stenosis, three of these restudied after valvoplasty, and 11 aortic stenosis). On the same day as the MR study, these patients underwent independent Doppler echocardiographic measurement of peak jet velocity. The results of 10 further MR investigations of aortic stenosis are also reported and compared with Doppler studies performed within 6 months. Of the 29 MR studies, 28 (97%) produced interpretable velocity maps, the one failure being attributed to misplacement of the imaging slice in a case of severe aortic stenosis. Agreement between MR and Doppler measurements of peak jet velocity in the recruited group was as follows: n = 18; range, 1.4-6.1 m/sec; mean, 3 m/sec; mean of differences (MR-Doppler), 0.23 m/sec; standard deviation of differences, 0.49 m/sec.

CONCLUSIONS
In vivo MR peak jet velocity measurements agree well with those made by Doppler ultrasound. The technique, which is not subject to restricted windows of access and has potential for further refinements, could contribute to improved evaluation of stenoses, especially at locations where ultrasonic access is limited.
Alteration of left ventricular endocardial function by intracavitary high-power ultrasound interacts with volume, inotropic state, and alpha 1-adrenergic stimulation.
Authors: De Hert S G , Gillebert T C , Brutsaert D L 
Published: June 2012

BACKGROUND
High-power intracavitary ultrasound abbreviates left ventricular (LV) ejection duration, thereby decreasing mechanical LV performance, presumably by selective impairment of endocardial endothelial function.

METHODS AND RESULTS
Effects of ultrasound were evaluated in the ejecting LV of anesthetized, open-chest dogs under different conditions of LV volume and contractile state and after mild selective alpha 1-adrenergic stimulation. LV pressures, left atrial pressures, and regional segment lengths were measured in anterior and posterior midwall. A cylindrical ultrasound probe (0.9 MHz, 25 W) mounted on a catheter was inserted into the LV cavity through the apex and was activated for 4 minutes in each condition. In protocol A (n = 7), LV volume was altered with caval vein occlusion and intravenous dextran infusion. The ultrasound probe was activated at low (4.1 +/- 0.9 mm Hg), mid (10.6 +/- 1.5 mm Hg), and high (17.9 +/- 1.8 mm Hg) LV end-diastolic pressure (EDP). Effects of ultrasound were less pronounced at higher EDP. For example, the time interval from end-diastole to peak (-)dP/dt decreased by 7.5 +/- 2.3% at low, 4.4 +/- 2.2% at mid, and 1.9 +/- 1.6% at high LVEDP (p < 0.001). In protocol B (n = 7), LV inotropic state was altered by slow intravenous infusion of low-dose calcium. The ultrasound probe was activated before and after calcium. Effects of ultrasound were less pronounced after calcium. Time from end-diastole to peak (-)dP/dt decreased by 8.4 +/- 3.1% at baseline and by 3.5 +/- 2.1% after calcium (p < 0.001). In protocol C (n = 7), activation of the ultrasound probe was performed at baseline and after mild selective alpha 1-adrenergic stimulation (propranolol plus phenylephrine). Effects of ultrasound were similar at baseline and after propranolol but increased after phenylephrine. Time from end-diastole to peak (-)dP/dt decreased by 5.2 +/- 2.4% at baseline, by 5.3 +/- 1.9% after propranolol, and by 8.9 +/- 3.2% after phenylephrine (p < 0.05).

CONCLUSIONS
Effects of intracavitary ultrasound, which are presumably mediated through modulation of endocardial endothelial function, were more important at low volume, lower calcium, and under mild selective alpha 1-adrenergic stimulation.