bluuebunny/crossref_metadata_2025 huggingface dataset:
Detection of dissection of the aortic intima and media after angioplasty of coarctation of the aorta. An angiographic, computer tomographic, and echocardiographic comparative study.
Authors: Erbel R , Bednarczyk I , Pop T , Todt M , Henrichs K J , Brunier A , Thelen M , Meyer J
Published: June 2011

Balloon coarctation angioplasty (BCA) was performed in eight patients (five male and three female) who were 14-49 years old (mean, 27.3 years) with isolated discrete unoperated coarctation of the aorta (n = 7) and postoperative recoarctation (n = 1). BCA was successful in seven of eight patients, resulting in a decrease in the gradient (64 +/- 19 to 16 +/- 13 mm Hg, p less than 0.01), an increase in the diameter at the coarctation site (0.9 +/- 0.4 to 1.6 +/- 0.4 mm, p less than 0.01). Follow-up (6 months) has demonstrated continued gradient relief (6 +/- 9 mm Hg) and diameter increase (1.6 +/- 0.2 cm). Monitoring was performed by transesophageal echocardiography (TEE) during BCA, and before and after BCA angiography and after BCA computed tomography. In three of seven patients, immediately distal to the BCA site, intimal flaps (1-2 cm) could be detected by TEE but not by angiography or computed tomography. Follow-up TEE showed spontaneous healing in two and persistence in one patient. By TEE and computed tomography in one of eight patients during follow-up, intima and media dissection was found with pleural effusion and spontaneous healing. In one female patient, aortic dissection occurred after successful uneventful BCA, detected by TEE at the 6-month follow-up study and subsequently confirmed by biplane angiography, not detected by computed tomography and previous monoplane angiography. Because of the significant morbidity of BCA in this group of patients, its role in the management of adults with coarctation has yet to be determined. Further long-term follow-up studies will demonstrate whether the observed intima and media dissection by TEE after BCA are related to aneurysm formation.
Peripartum myocarditis and cardiomyopathy.
Authors: Midei M G , DeMent S H , Feldman A M , Hutchins G M , Baughman K L
Published: June 2011

The clinical and pathologic features of 18 consecutive patients with peripartum cardiomyopathy at The Johns Hopkins Hospital were examined in an attempt to define the incidence of myocarditis and to determine its response to immunosuppressive agents. In addition to routine studies, patients were evaluated with echocardiography, nuclear ventriculography, right heart catheterization, and myocardial biopsy. Fourteen of the 18 patients (78%) showed evidence of myocarditis. Of these, 10 were treated with immunosuppressive therapy. Nine of the 10 treated patients with myocarditis had subjective and objective improvement. Follow-up endomyocardial biopsies in these patients showed resolution or substantial improvement in myocarditis. Four patients with myocarditis not treated with immunosuppressives also improved. All patients improving spontaneously presented with congestive heart failure within 1 month of delivery and improved dramatically within days of presentation. Four of the 18 patients showed no evidence of myocarditis. Of these, two improved, and two deteriorated (both requiring cardiac transplantation). None of these four patients were treated with immunosuppressive therapy. We conclude that in patients with peripartum cardiomyopathy, 1) the etiology remains unclear although myocarditis was present in 78% of those with this condition, 2) resolution of myocarditis is associated with significant improvement in left ventricular function, 3) myocarditis may resolve spontaneously without detectable loss of cardiac function, and 4) immunosuppressive therapy in patients with myocarditis and persistent left ventricular dysfunction may improve left ventricular function and prognosis.
Left ventricular hypertrophy and impaired diastolic filling in essential hypertension. Diastolic mechanisms for systolic dysfunction during exercise.
Authors: Cuocolo A , Sax F L , Brush J E , Maron B J , Bacharach S L , Bonow R O
Published: June 2011

Left ventricular ejection fraction is normal at rest but may respond abnormally to exercise in many patients with essential hypertension. To assess the determinants of the abnormal ejection fraction response to exercise, we performed radionuclide angiography at rest and during exercise in 41 hypertensive patients without coronary artery disease. In 22 patients (group 1), the ejection fraction increased more than 5% during exercise; in the other 19 patients (group 2), the ejection fraction either increased by less than 5% or decreased with exercise. Left ventricular diastolic filling was impaired at rest in patients in group 2 compared with group 1, with reduced peak filling rate (2.5 +/- 0.4 vs. 3.1 +/- 0.7 end-diastolic volume/sec; p less than 0.01) and prolonged time to peak filling rate (175 +/- 28 vs. 153 +/- 22 msec; p less than 0.01). Impaired diastolic filling in group 2 was associated with less augmentation in end-diastolic volume during exercise compared with group 1 (p less than 0.01). These observations were not dependent on the threshold value that was arbitrarily chosen to define an abnormal ejection fraction response, as there were significant correlations for the entire group between the magnitude of change in ejection fraction with exercise and both the resting peak filling rate (r = 0.46) and the change in end-diastolic volume with exercise (r = 0.62).(ABSTRACT TRUNCATED AT 250 WORDS)
Reversible segmental left ventricular dysfunction after coronary angioplasty.
Authors: van den Berg E K , Popma J J , Dehmer G J , Snow F R , Lewis S A , Vetrovec G W , Nixon J V
Published: June 2011

Patients with chronic segmental myocardial dysfunction may demonstrate improvement after coronary revascularization. To evaluate the early effects of percutaneous transluminal coronary angioplasty (PTCA) on resting left ventricular segmental function, we obtained serial two-dimensional echocardiograms 1.1 +/- 0.9 days before and 3.1 +/- 2 days after elective PTCA in 40 patients. Echocardiograms were reviewed in a blind fashion; left ventricular segmental wall motion was analyzed in four short-axis views, and a score was assigned to each region (0, normal; 1, hypokinetic; and 2, akinetic). Abnormal regional wall motion was present in 20 of the patients before PTCA. Summed segment scores in these 20 patients showed an improvement in regional wall motion from 4.5 +/- 2.5 to 1.6 +/- 2.1 (p less than 0.01) after successful PTCA. Similar results were obtained when the patients were divided into those with or without a previous myocardial infarction. Improvement occurred in the seven patients without a previous myocardial infarction; the summed segment score decreased from 4.2 +/- 3.4 to 0.86 +/- 1.6 (p less than 0.05) after PTCA. Ten of the 13 patients with a prior myocardial infarction demonstrated improvement in wall motion after PTCA; the summed segment scores decreased 54% (p less than 0.001). Of the 260 segments analyzed in the study, 180 were normal before and after PTCA. Forty-nine of the 69 hypokinetic segments were normal, and 10 of 12 akinetic segments were hypokinetic after successful coronary revascularization. There was no deterioration in wall motion after PTCA.(ABSTRACT TRUNCATED AT 250 WORDS)
Decreased magnitude of heart rate spectral components in coronary artery disease. Its relation to angiographic severity.
Authors: Hayano J , Sakakibara Y , Yamada M , Ohte N , Fujinami T , Yokoyama K , Watanabe Y , Takata K
Published: June 2011

We analyzed the spectral components of RR interval variability under controlled respiration (15 breaths/min) in 56 patients (age range, 35-73 years) referred for coronary angiography; 14 patients had multivessel disease (group M), 21 had one-vessel disease (group S), and 21 had nonsignificant disease or normal coronary artery (group N). There were 43 healthy controls (age range, 36-71 years) (group C). The patients had no clinical evidence of heart failure, hypertension, diabetes mellitus, or acute stage of infarction and had taken no medication for 3 days. The autoregressive power spectral density of RR interval variability contains two major components, respiratory sinus arrhythmia (RSA) (0.25 Hz) and Mayer wave-like sinus arrhythmia (MWSA) (0.04-0.15 Hz), which have magnitudes that are quantitative markers of cardiac vagal activity and sympathetic activity with vagal modulation, respectively. We represented the magnitudes by the coefficient of component variance (CCV), which provided the amplitude relative to the mean RR interval. The age- and sex-adjusted mean of CCVRSA significantly decreased with advancing angiographic severity (1.64 +/- 0.09%, 1.66 +/- 0.12%, 1.22 +/- 0.13%, and 0.81 +/- 0.16% for groups C, N, S, and M, respectively) (p = 0.0001). The CCVRSA was unrelated to left ventricular function, previous myocardial infarction, or stenosis of any specific artery including the sinoatrial and atrioventricular node arteries. The CCVMWSA decreased only in group M (p = 0.0462). These results indicate that coronary artery disease is associated with vagal dominant impairment in autonomic cardiac function and that reduction in the vagal cardiac function correlates with the angiographic severity.
Dissociation of end systole from end ejection in patients with long-term mitral regurgitation.
Authors: Brickner M E , Starling M R
Published: June 2011

To determine whether left ventricular (LV) end systole and end ejection uncouple in patients with long-term mitral regurgitation, 59 patients (22 control patients with atypical chest pain, 21 patients with aortic regurgitation, and 16 patients with mitral regurgitation) were studied with micromanometer LV catheters and radionuclide angiograms. End systole was defined as the time of occurrence (Tmax) of the maximum time-varying elastance (Emax), and end ejection was defined as the time of occurrence of minimum ventricular volume (minV) and zero systolic flow as approximated by the aortic dicrotic notch (Aodi). The temporal relation between end systole and end ejection in the control patients was Tmax (331 +/- 42 [SD] msec), minV (336 +/- 36 msec), and then, zero systolic flow (355 +/- 23 msec). This temporal relation was maintained in the patients with aortic regurgitation. In contrast, in the patients with mitral regurgitation, the temporal relation was Tmax (266 +/- 49 msec), zero systolic flow (310 +/- 37 msec, p less than 0.01 vs. Tmax), and then, minV (355 +/- 37 msec, p less than 0.001 vs. Tmax and p less than 0.01 vs. Aodi). Additionally, the average Tmax occurred earlier in the patients with mitral regurgitation than in the control patients and patients with aortic regurgitation (p less than 0.01, for both), whereas the average time to minimum ventricular volume was similar in all three patient groups. Moreover, the average time to zero systolic flow also occurred earlier in the patients with mitral regurgitation than in the control patients (p less than 0.01) and patients with aortic regurgitation (p less than 0.05). Because of the dissociation of end systole from minimum ventricular volume in the patients with mitral regurgitation, the end-ejection pressure-volume relations calculated at minimum ventricular volume did not correlate (r = -0.09), whereas those calculated at zero systolic flow did correlate (r = 0.88) with the Emax slope values. We conclude that end ejection, defined as minimum ventricular volume, dissociates from end systole in patients with mitral regurgitation because of the shortened time to LV end systole in association with preservation of the time to LV end ejection due to the low impedance to ejection presented by the left atrium. Therefore, pressure-volume relations calculated at minimum ventricular volume might not be useful for assessing LV chamber performance in some patients with mitral regurgitation.
Effect of epicardial patch electrodes on transthoracic defibrillation.
Authors: Lerman B B , Deale O C
Published: June 2011

To improve survival rates in patients undergoing surgical ablative procedures for malignant ventricular tachycardia (VT), a frequent practice is to implant epicardial patch electrodes at the time of map-guided surgery. After operation, patients with inducible VT often receive an automatic internal cardioverter/defibrillator (AICD) implant, whereas patients with noninducible VT usually do not. In the event that spontaneous, hypotensive VT or ventricular fibrillation should subsequently occur in the patient with noninducible VT, however, transthoracic defibrillation and resuscitation may prove difficult, because the patch electrodes are insulated with silicone rubber that can reduce the amount of current traversing the myocardium and thus can increase transthoracic defibrillation threshold (DFT). In this study, DFT was determined in mongrel dogs to test the hypothesis that epicardial patch electrodes elevate threshold. This study was also designed to assess the effect of patch electrode orientation and size on DFT. In the first protocol (perpendicular orientation), small epicardial patch electrodes (surface area, 30 cm2) were sutured to the epicardial surfaces of the anterior right and posterior left ventricles in 15 dogs so that the center axes of the patch electrodes were coincident and perpendicular to the coincident center axes of the transthoracic electrodes. The effect of two large epicardial patch electrodes (surface area, 53 cm2) on transthoracic DFT was also examined in eight of these dogs. In the second protocol (parallel orientation), small patch electrodes were sutured to the lateral surfaces of the right and left ventricles in seven dogs.(ABSTRACT TRUNCATED AT 250 WORDS)
Effect of endothelin-1 in man.
Authors: Vierhapper H , Wagner O , Nowotny P , Waldhäusl W
Published: June 2011

The effect of an intravenous infusion of human endothelin-1 on blood pressure and plasma concentrations of endothelin-1, potassium, sodium, renin, aldosterone, and atrial natriuretic factor was investigated in six healthy, sodium-loaded men. During the peptide's exogenous application (1.0, 2.5, and 5.0 ng/kg.min), its plasma concentrations rose from a basal value of 1.2 +/- 0.3 to 3.2 +/- 1.9, 9.9 +/- 7.6, and 56.5 +/- 50.3 pmol/l (p less than 0.01), respectively, and mean blood pressure rose from a basal value of 87.1 +/- 7.3 to 92.6 +/- 8.2 mm Hg (p less than 0.01). A rise in serum concentrations of potassium (from 4.0 +/- 0.3 to 4.6 +/- 0.2 mmol/l; p less than 0.005) and a concomitant fall in serum concentrations of sodium (from 142.7 +/- 1.0 to 139.5 +/- 2.3 mmol/l; p less than 0.05) was seen in each subject. Plasma concentrations of renin, aldosterone, and atrial natriuretic factor did not change during the infusion of endothelin-1. Thus, in the doses used, endothelin-1 induces a rise in blood pressure and serum potassium concentrations.
Black-white differences in exercise blood pressure. The Lipid Research Clinics Program Prevalence Study.
Authors: Ekelund L G , Suchindran C M , Karon J M , McMahon R P , Tyroler H A
Published: June 2011

After exclusion of persons on blood pressure medication or with prevalent cardiovascular disease, we studied 83 black and 2,548 white men and 113 black and 1,519 white women 20-69 years old from the Lipid Research Clinics population sample who had performed a standardized treadmill exercise test. Resting systolic and diastolic blood pressures were similar in black and white men, but the diastolic pressure was significantly higher in black than in white women (81.4 vs 77.4 mm Hg). Body weight was higher in black than in white women, and reported physical activity was higher in black than in white men. The proportion of smokers was somewhat higher in blacks than in whites. During the treadmill exercise test with a modified Bruce protocol, mean systolic blood pressure at stage 2 was 174 mm Hg in black men and 166 mm Hg in white men (p less than 0.02), but stage 2 blood pressures did not differ between black and white women (153 and 152 mm Hg, respectively). Even after adjustments were made for levels of baseline characteristics (age, weight, resting systolic blood pressure, smoking, low density lipoprotein cholesterol, physical activity, and alcohol intake), black men responded with a 7-mm Hg higher systolic blood pressure during exercise than white men (p less than 0.01). Another new finding was a highly significant positive association between stage 2 systolic blood pressure and low density lipoprotein cholesterol in men. The findings suggest a higher systemic vascular resistance during exercise in the selected sample of black men, which is consistent with the higher incidence of hypertension in black men.
Validation of [1-11C]acetate as a tracer for noninvasive assessment of oxidative metabolism with positron emission tomography in normal, ischemic, postischemic, and hyperemic canine myocardium.
Authors: Armbrecht J J , Buxton D B , Schelbert H R
Published: June 2011

Extraction and clearance kinetics of [1-11C]acetate were examined in 65 experiments in 30 open-chest dogs. Twenty-nine studies were performed at control, 13 during ischemia, eight after reperfusion, 13 during dipyridamole-induced hyperemia, and two during alteration of cardiac workload. [1-11C]Acetate was injected directly into the left anterior descending coronary artery, and myocardial tissue-time activity curves were recorded with a gamma probe. The single-pass extraction fraction averaged 64.2 +/- 9.7% in control, 65.3 +/- 9.1% in ischemia, 70.0 +/- 4.4% in reperfusion, and 46.5 +/- 7.4% in dipyridamole-induced hyperemia groups. 11C clearance was biexponential in all cases. The rate constant k1 for the first rapid clearance phase correlated closely with myocardial oxygen consumption (r = 0.94) in control, ischemia, reperfusion, and dipyridamole-induced hyperemia groups. Monoexponential fitting of only the first linear part of the clearance curve yielded the rate constant kmono, which also correlated with myocardial oxygen consumption (r = 0.96). Arterial lactate concentrations and the amount of free fatty acid oxygen equivalents consumed by the myocardium were shown to have a small but statistically significant impact on the relation between [1-11C]acetate clearance rate constants and myocardial oxygen consumption. The fraction of 14CO2 activity contributing to overall 14C activity leaving the myocardium after simultaneous injection of [1-14C]acetate (n = 24) was relatively high in all cases (97.4 +/- 2.5% in control, 89 +/- 2.6% in ischemia, 94.1 +/- 3.5% in reperfusion, and greater than 99% in dipyridamole groups), indicating that externally measured 11C clearance corresponds to CO2 production and thus to tricarboxylic acid cycle activity. In conclusion, the results validate the use of [1-11C]acetate as a tracer of oxidative myocardial metabolism for use with positron emission tomography.
Estrogen modulates responses of atherosclerotic coronary arteries.
Authors: Williams J K , Adams M R , Klopfenstein H S
Published: June 2011

Although evidence indicates that estrogen replacement therapy reduces risk of coronary heart disease, the mechanism remains unknown. Among the possibilities are that estrogen replacement therapy may 1) inhibit growth of atherosclerotic plaque and 2) decrease the prevalence of transient myocardial ischemia and myocardial infarction by modulating vasomotion in atherosclerotic coronary arteries. Using quantitative coronary angiography, we determined vasomotor responses of atherosclerotic coronary arteries in ovariectomized cynomolgus monkeys; six were given physiological estrogen "replacement" by subcutaneous implants, and six were not. Intracoronary infusion of the endothelium-dependent dilator acetylcholine (1 X 10(-6) M) caused paradoxical constriction of coronary arteries (from 1.2 +/- 0.2 to 0.6 +/- 0.1 mm, p less than 0.05) in the estrogen-deficient monkeys. However, acetylcholine tended to minimally dilate the left circumflex coronary artery in estrogen-treated monkeys (from 1.2 +/- 0.2 to 1.5 +/- 0.2 mm, p greater than 0.2). Although estrogen replacement therapy reduced plaque extent in coronary arteries, altered vasomotion was not related to plaque extent. We conclude that estrogen modulates vasomotion of atherosclerotic coronary arteries of monkeys and speculate that estrogen-modulated constrictor responses of atherosclerotic coronary arteries may reduce the incidence of coronary heart disease in postmenopausal women.
Prolonged duration of myocardial ischemia in patients with coronary heart disease and impaired cardiopulmonary baroreceptor sensitivity.
Authors: Trimarco B , Chierchia S , Lembo G , De Luca N , Ricciardelli B , Condorelli G , Volpe M , Condorelli M
Published: June 2011

To investigate the potential contribution of cardiopulmonary reflexes in myocardial ischemia, the coronary vascular response to cardiopulmonary baroreceptor unloading and the number and the duration of spontaneous episodes of symptomatic and asymptomatic myocardial ischemia were evaluated in 23 patients with coronary heart disease. Lower-body negative pressure at -10 mm Hg, which causes selective deactivation of cardiopulmonary receptors, reduced left ventricular filling pressure in all patients, but calculated coronary vascular resistance increased in only 14 patients (from 0.846 +/- 0.1 to 1.07 +/- 0.1 mm Hg/ml/min, p less than 0.01) (group 1). In the remaining nine patients, coronary resistance did not change during cardiopulmonary receptor unloading (group 2). A 60-mm Hg increase in neck tissue pressure, which induces arterial baroreflex-mediated sympathetic activation, caused comparable coronary vasoconstriction in the two groups. Clinical characteristics of the two groups were similar, except that a lower ejection fraction was measured in group 1 (45 +/- 2% vs. 56 +/- 1%, p less than 0.01). In the 14 patients in group 1, 24-hour electrocardiographic monitoring showed 151 episodes of myocardial ischemia (average individual value, 10.8 +/- 1), 137 of which were asymptomatic, with an individual daily ischemic period of 62 +/- 6 minutes. In contrast, the nine patients in group 2 had only symptomatic episodes of myocardial ischemia, and the daily ischemic period in these patients was longer than in patients of group 1 (104 +/- 10 minutes, p less than 0.01). After a 3-day treatment with digitalis, the patients of group 2 showed 38 asymptomatic episodes of myocardial ischemia and a shorter daily ischemic period (85 +/- 6 minutes, p less than 0.01 vs. control conditions). In contrast, no change in number and duration of the ischemic episodes was detected in group 1. The effects of acute administration of digitalis (Lanatoside-C 0.02 mg/kg body wt e.v.) on the coronary vascular response to cardiopulmonary receptor unloading were assessed in a separate group of patients with ischemic heart disease. Digitalis treatment did not significantly modify the magnitude of the coronary vascular response induced by -10 mm Hg lower-body negative pressure in the patients showing in control conditions an increase of coronary vascular resistance greater than 20% of the basal value during cardiopulmonary receptor unloading. On the contrary, digitalis potentiated the coronary reflex response to -10 mm Hg lower-body negative pressure in the patients with impaired cardiopulmonary responsiveness (delta percent increase in coronary vascular resistance: 1 +/- 1% in control conditions; 23 +/- 3.9% after digitalis, p less than 0.001).(ABSTRACT TRUNCATED AT 400 WORDS)
Combined effects of nitrates on the coronary and peripheral circulation in exercise-induced ischemia.
Authors: De Coster P M , Chierchia S , Davies G J , Hackett D , Fragasso G , Maseri A
Published: June 2011

We compared the effects of isosorbide dinitrate (ISDN) administered by intracoronary and intravenous routes in 10 patients with severe coronary artery disease, stable effort angina, and very low exercise tolerance. Supine bicycle ergometer exercise was performed under four conditions: 1) control, 2) after intracoronary administration of 0.4 mg ISDN, 3) 1 hour later (control 2), and 4) after administration of intravenous 4 mg ISDN. At rest, intracoronary ISDN caused no significant hemodynamic effects, whereas intravenous infusion of ISDN resulted in a decline in left ventricular (LV) systolic pressure (-20 +/- 5 mm Hg), LV end-diastolic volume (-27 +/- 3%), and LV end-systolic volume (-30 +/- 4%). After intracoronary infusion of ISDN, ST segment depression and the increase in LV end-diastolic pressure and LV end-systolic volume induced by exercise were significantly less abnormal than during control (0.20 +/- 0.09 vs. 0.14 +/- 0.08 mV, 36 +/- 7 vs. 24 +/- 8 mm Hg, and 91 +/- 40% vs. 40 +/- 29%, respectively). When exercise was performed after intravenous infusion of ISDN, the above-mentioned parameters were significantly improved even further: ST segment depression to 0.05 +/- 0.07 mV, end-diastolic pressure to 14 +/- 7 mm Hg, and LV end-systolic volume to 5 +/- 11% (all p less than 0.01 compared with intracoronary ISDN). Thus, in patients with severe coronary artery disease, it is suggested that intracoronary nitrates increase coronary blood supply during effort-induced ischemia, based on significant improvements in the indirect measures of ST segment depression, LV end-diastolic pressure, and LV volume.(ABSTRACT TRUNCATED AT 250 WORDS)
Early afterdepolarizations induced in vivo by reperfusion of ischemic myocardium. A possible mechanism for reperfusion arrhythmias.
Authors: Priori S G , Mantica M , Napolitano C , Schwartz P J
Published: June 2011

Recent studies in vitro have shown that afterdepolarizations may develop during reperfusion after hypoxia, thus suggesting that these afterdepolarizations may contribute to the genesis of reperfusion arrhythmias. We recorded monophasic action potentials (MAPs) during myocardial ischemia and reperfusion to investigate whether afterdepolarizations develop in vivo when reperfusion arrhythmias occur. In 15 anesthetized cats, 24 trials of 10 minutes of occlusion of the left anterior descending coronary artery were followed by reperfusion. In 13 of 24 (54%) trials, afterdepolarizations developed at the moment of reperfusion, with a mean amplitude of 2.4 +/- 1.1 mV (13 +/- 8% of MAP amplitude). When cycle length was either increased by vagal stimulation or decreased by atrial pacing, early afterdepolarization (EAD) amplitude was modified, according to what has been described for EAD in vitro, with a positive linear correlation between cycle length and EAD amplitude (r = 0.91, p less than 0.0001). The occurrence of EAD was not related to rapid changes in left ventricular pressure. In the eight of 13 (62%) cases in which EAD development was associated with reperfusion arrhythmias, the coupling interval of the EAD and of premature ventricular contractions showed a significant correlation (r = 0.86, p less than 0.0001). However, in five of 13 (38%) cases, occurrence of reperfusion arrhythmias was not accompanied by the presence of EAD on the MAP recording. In two animals, a 2:1 block of EAD conduction was observed, and this was reflected on the intracavitary electrocardiogram as T wave alternans. Thus, EADs occur frequently after reperfusion in vivo, with a time course that parallels the onset of reperfusion arrhythmias. This finding further supports the role of triggered activity in the genesis of reperfusion arrhythmias in vivo.
Alteration of endothelium-dependent distribution of myocardial blood flow after coronary occlusion and reperfusion.
Authors: Pelc L R , Garancis J C , Gross G J , Warltier D C
Published: June 2011

We have previously demonstrated that intracoronary infusion of the endothelium-dependent vasodilators acetylcholine, ATP, or arachidonic acid produces a preferential increase in subendocardial blood flow in anesthetized dogs. This study was performed to assess the effects of coronary artery occlusion and reperfusion on the distribution of myocardial blood flow produced by endothelium-dependent and endothelium-independent vasodilators. The endothelium was damaged by occlusion of the left anterior descending coronary artery for 45 minutes followed by 60 minutes of reperfusion in pentobarbital-anesthetized dogs. Intracoronary infusions of the endothelium-dependent vasodilators acetylcholine, bradykinin and thiazolylethylamine or the endothelium-independent vasodilator sodium nitroprusside were performed, and regional myocardial blood flow (by radioactive microspheres) was measured before and after occlusion and reperfusion. There were no changes in systemic hemodynamics during intracoronary infusion of vasodilators before or after coronary occlusion and reperfusion. All vasodilators produced similar increases in transmural blood flow before occlusion; however, only the endothelium-dependent vasodilators produced a significant increase in the subendocardial-to-subepicardial blood flow ratio. Increases in transmural flow as well as the preferential increase in subendocardial blood flow produced by acetylcholine, bradykinin, and thiazolylethylamine were attenuated after coronary occlusion and reperfusion. In contrast, increases in transmural blood flow produced by sodium nitroprusside were unchanged. These results suggest that the preferential increase in subendocardial perfusion produced by acetylcholine, bradykinin, and thiazolylethylamine is endothelium-dependent and may be selectively modified by ischemic insult.
Effect of coronary stenosis on myocardial blood flow during exercise in the chronically pressure-overloaded hypertrophied left ventricle.
Authors: Bache R J , Wright L , Laxson D D , Dai X Z
Published: June 2011

This study was performed to determine if a coronary artery stenosis would result in more-severe perfusion abnormalities in hypertrophied compared with normal canine hearts during exercise. Studies were performed in eight normal control dogs and in seven adult dogs in which a 67% increase in left ventricular mass wa produced by banding the ascending aorta at 9 weeks of age. Myocardial blood flow was measured by the microsphere method during treadmill exercise in the presence of a coronary artery stenosis that decreased distal coronary perfusion pressure to 55 or 42 mm Hg. At a coronary pressure of 55 mm Hg, mean myocardial blood flow was decreased by 23 +/- 5% in normal control dogs but was decreased by 53 +/- 10% in dogs with left ventricular hypertrophy (LVH) (p less than 0.05, comparing normal vs. LVH dogs). Similarly, at a coronary pressure of 42 mm Hg, mean blood flow was decreased by 53 +/- 6% below control in normal dogs but was decreased by 76 +/- 5% below control values in dogs with LVH (p less than 0.01, comparing normal vs. LVH dogs). In both groups of dogs, the stenosis caused a gradient of hypoperfusion, worsening from epicardium to endocardium. However, for each level of stenosis, subendocardial blood flow and the ratio of subendocardial to subepicardial blood flow was less in LVH than in normal canine hearts. These findings demonstrate that the presence of LVH secondary to long-term pressure overload is associated with an increased vulnerability to myocardial hypoperfusion during exercise in the presence of a coronary artery stenosis.
Computerized tabulation of cine coronary angiograms. Its implication for results of randomized trials.
Authors: Favaloro R G
Published: June 2011

The quality of cine angiography is excellent in our days, and as a consequence some of the pitfalls encountered in previous randomized trials are not currently present. An example can be found in the CASS analysis of the reproducibility of coronary arteriographic reading by the Quality Control Committee Sessions: "There is an indication that different clinics" involved in the CASS trial "can reduce the variability between their readings by concerted effort to improve both the quality and the completeness of the angiographic examination." The introduction of electronic calipers to judge the severity of the obstruction can eliminate human errors. The computerized protocol has the disadvantage that it takes longer to tabulate cine coronary angiography and it will depend on its pattern, but it certainly will not be as long as filling in the CASS protocol. However, this effort is justified because it will enrich our knowledge of coronary arteriosclerosis. As a result, patients will be divided into proximal (1, 2, 12, 13, and 19), middle (mainly, 3, 14, and 20), and distal (remainder) segments. Sometimes midsegments can be important. For example, in the report from CASS related to the left main equivalent lesions, the 5-year survival rate was 48% if the obstruction on the left anterior descending was proximal and increased to 71% if it was more distal. Several randomized studies to compare PTCA with CABG as suggested by Gruentzig et al in 1979 are underway, and it is hoped that the data will be properly analyzed. However, if cine coronary angiography and the status of the left ventricle are not carefully tabulated (classification of patients into left main trunk or one-, two-, or three-vessel disease is not sufficient), the results of the randomized trials comparing PTCA with CABG will add more confusion instead of clarifying proper therapeutic implications.
Effect of age on the in vitro reflection coefficient of the aortoiliac bifurcation in humans.
Authors: Greenwald S E , Carter A C , Berry C L
Published: June 2011

The local reflection coefficient (r) at the aortoiliac junction was estimated in vessels removed at autopsy from 15 females and 31 males aged 2 months to 88 years by calculating the characteristic impedance (Zc) of the abdominal aorta and the two common iliac arteries. Zc was evaluated for each vessel by measuring cross-sectional area from radiographs and propagation velocity of an isolated pressure impulse generated by a solenoid-driven piston connected to the distal end of the abdominal aorta, and detected at several sites a known distance from the junction. Attenuation coefficients in the aorta were estimated from the peak amplitude of the impulse at these several sites. We observed significant decreases with age in abdominal aortic attenuation coefficient (gamma = 0.053-5 x 10(-4) age [yr], r = -0.42, p less than 0.005), and the area ratio (AR) of the junction (sum of the iliac cross-sectional areas/aortic cross-sectional area) (AR = 0.93-0.002 x age [yr], r = -0.31, p less than 0.05). Bifurcation angle (Angle) and aortic propagation velocity (caorta) increased significantly (angle = 40.2 + 0.26 x age [yr], r = 0.41, p less than 0.01; caorta (ms-1) = 7.59 + 0.175 x age [yr], r = 0.69, p less than 0.0001). No significant association between age and iliac propagation velocity was found. On the basis of area measurements alone, it has been argued that the observed decrease in area ratio with age causes r to become more positive. The lack of age-related changes in iliac propagation velocity (and hence stiffness), an observation confirmed by most of the few reports in the literature, and the large increase in abdominal aortic stiffness, however, greatly outweighed the area ratio changes and caused a significant decline in reflection coefficient from +0.3 in early life to -0.3 in old age. (Reflection coefficient = 0.30-0.0065 x age [yr], r = -0.68, p less than 0.0001). Between the ages of 30 and 60 years, its absolute value was less than 0.1, confirming in vivo work on subjects within this age range. In children, a significant positive reflection at the distal end of the aorta will amplify the pulse wave in this region. As this vessel becomes stiffer with increasing age, amplification will increase, whereas the increasingly negative value of r will partially offset this rise, reducing pulse pressure on either side of the junction.(ABSTRACT TRUNCATED AT 400 WORDS)
Granulocyte activation after coronary angioplasty in humans.
Authors: De Servi S , Mazzone A , Ricevuti G , Fioravanti A , Bramucci E , Angoli L , Stefano G , Specchia G
Published: June 2011

To determine whether percutaneous transluminal coronary angioplasty (PTCA) would lead to neutrophil activation with subsequent discharge of proteolytic enzymes, like elastase, and oxygen free radicals, like superoxide anion, blood samples were taken from the coronary sinus and aorta in 14 patients with stable angina and one-vessel disease who underwent PTCA. Neutrophils were separated by means of the Ficoll-Hypaque system and were stimulated to detect release of elastase and generation of superoxide anion. Plasma levels of elastase were also measured by an immunoenzymatic method. PTCA was successful in all patients. Plasma elastase levels increased significantly at the end of the procedure compared with pre-PTCA values both in the coronary sinus (from 129.2 +/- 16.6 to 286.6 +/- 39.7 micrograms/l, p less than 0.005) and in the aorta (from 117.4 +/- 13.6 to 258.1 +/- 41.3 micrograms/l, p less than 0.005). On the other hand, superoxide anion released in the supernatants after neutrophil stimulation by phorbol-myristate-acetate decreased after PTCA in the coronary sinus (before PTCA, 60.1 +/- 7.1; after PTCA, 40.7 +/- 6.8 nmol 1 x 10(7) granulocytes/ml/15 min, p less than 0.05), whereas a mild but not significant decrease was observed in the aorta (from 58.3 +/- 10.9 to 55.3 +/- 8.6 nmol 1 x 10(7) granulocytes/ml/15 min, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
Attenuated forearm vasodilative response to intra-arterial atrial natriuretic peptide in patients with heart failure.
Authors: Hirooka Y , Takeshita A , Imaizumi T , Suzuki S , Yoshida M , Ando S , Nakamura M
Published: June 2011

It has been shown that renal responses to atrial natriuretic peptide (ANP) are markedly attenuated in patients with heart failure. This study aimed to determine if vasodilative response to ANP is altered in patients with heart failure. In patients with heart failure (n = 7) and age-matched normal subjects (n = 7), forearm blood flow was measured using a strain-gauge plethysmograph during intra-arterial infusion of alpha-human ANP (50, 100, 200, and 400 ng/min) or nitroglycerin (100, 200, 400, and 600 ng/min). Forearm vasodilatation evoked with intra-arterial alpha-human ANP in patients with heart failure was considerably less (p less than 0.01) than that in normal subjects. In contrast, nitroglycerin produced comparable forearm vasodilatation in the two groups. Plasma ANP and cyclic guanosine monophosphate (GMP) levels at rest were higher in patients with heart failure than in normal subjects (p less than 0.05 for both), but the increases in plasma ANP and cyclic GMP in the venous effluents during intra-arterial ANP infusion did not differ between the two groups. These results indicate that the direct vasodilative effect of ANP on forearm vessels was attenuated in patients with heart failure as compared with that in normal subjects. The mechanisms responsible for this alteration are not clear but might involve mechanisms other than down-regulation of the ANP receptors because the increases in venous plasma cyclic GMP caused by intra-arterial ANP were comparable between patients with heart failure and normal subjects.
Inhibition of clot-bound alpha 2-antiplasmin enhances in vivo thrombolysis.
Authors: Reed G L , Matsueda G R , Haber E
Published: June 2011

Recent experiments in vitro have shown that inhibition of human alpha 2-antiplasmin by a monoclonal antibody (MAb RWR) markedly enhances clot lysis by plasminogen activators. To extend these studies in vivo, we tested whether inhibition of clot or fibrin-bound alpha 2-antiplasmin by MAb RWR could enhance the lysis of a human clot by tissue-type plasminogen activator (t-PA) in a rabbit jugular vein thrombosis model. Compared with a saline placebo or a control antibody, MAb RWR significantly increased thrombolysis by endogenous plasminogen activator in rabbits to which no t-PA was administered (p less than 0.05). In rabbits that received t-PA, the combination of MAb RWR and t-PA caused significantly greater thrombolysis than equivalent doses of t-PA alone (p less than 0.05). However, compared with equipotent doses of t-PA alone, the combination of MAb RWR and t-PA did not increase the nonspecific consumption of fibrinogen. These experiments suggest that the combination of an alpha 2-antiplasmin inhibitor and a plasminogen activator could be a more potent thrombolytic strategy.
Dietary fish oil accelerates the response to coronary thrombolysis with tissue-type plasminogen activator. Evidence for a modest platelet inhibitory effect in vivo.
Authors: Braden G A , Knapp H R , Fitzgerald D J , FitzGerald G A
Published: June 2011

To assess the platelet inhibitory effect of high doses of fish oils and relate it to alterations in eicosanoid synthesis, we used a canine model in which coronary thrombosis, the time to reperfusion induced by recombinant tissue-type plasminogen activator (rt-PA), and the rate of spontaneous reocclusion are sensitive to platelet inhibition. In the animals fed fish oil, the time to rt-PA induced thrombolysis was accelerated (mean, 63 vs. 27 minutes; p less than 0.003). The time to thrombotic occlusion and the rate of reocclusion were unaltered. The ratio of eicosapentaenoic acid (EPA) to arachidonic acid rose in platelet and endothelial cell membranes, whereas serum thromboxane (Tx) B levels fell a mean 86%, and basal excretion of 2,3-dinor-TxB2 (TxA2-M) declined. Basal prostaglandin (PG) I2 formation was unaltered, whereas biosynthesis of EPA-derived TxA3 and PGI3 increased. In control animals, TxA2 formation increased during thrombosis; there was a further, more marked rise during reperfusion. PGI2 formation also increased, probably as a response to platelet-vascular interactions. Stimulated production of both eicosanoids was strikingly suppressed in the animals fed fish oil. Fish oils significantly enhance the efficacy of rt-PA in vivo, albeit to a modest extent. Because the time to reperfusion is highly sensitive to Tx-dependent platelet activation, this effect is likely to reflect the demonstrated suppression of TxA2 biosynthesis by fish oils.
Alpha-adrenoceptor stimulation and blockade modulates cesium-induced early afterdepolarizations and ventricular tachyarrhythmias in dogs.
Authors: Ben-David J , Zipes D P
Published: June 2011

In 84 open-chest dogs, we studied the effects on early afterdepolarizations (EADs) and ventricular tachyarrhythmias (VTs) induced by cesium chloride (168 mg/kg i.v.) of alpha-adrenoceptor stimulation with phenylephrine (100 micrograms plus 0.25 microgram/kg/min i.v.) and with left ansa subclavia stimulation (LAS; 2 Hz, 4 msec, 2 mA) after propranolol (0.5 mg/kg) administration. We also studied the effects of alpha-adrenoceptor blockade with phentolamine (3 mg/kg), prazosin (25-500 micrograms/kg), yohimbine (10-500 micrograms/kg), WB 4101 (2 mg/kg), and benoxathian (2 mg/kg) during decentralized LAS. EAD amplitude, presented as a percentage of monophasic action potential amplitude, was recorded simultaneously with contact electrodes from the right and left ventricular endocardium. Phenylephrine and LAS plus propranolol increased EAD amplitude (31.5 +/- 8.8% to 47.8 +/- 9.7% and 34.8 +/- 4.1% to 46.1 +/- 6.4%, respectively) and the prevalence of VT (from three to nine of 11 dogs and from the three to five of six dogs, respectively). Prazosin produced a dose-response decrease in EAD amplitude and reduced the prevalence of VT. Yohimbine did not alter the amplitude of EADs or the prevalence of VT. WB 4101 and phentolamine reduced the amplitude of EADs produced by cesium and LAS (from 44.3 +/- 10.2% to 32.6 +/- 9.4% and from 39.8 +/- 6.9% to 30.3 +/- 6.3%, respectively) and the prevalence of VT (from eight to one of 10 dogs and from 13 to 5 of 20 dogs, respectively). Benoxathian did not alter significantly the amplitude of EADs (41.6 +/- 11.4% to 37.5 +/- 9.4%) or the prevalence of VT (from six to five of 10 dogs).(ABSTRACT TRUNCATED AT 250 WORDS)
Premature escape beats induced by overdrive pacing in canine Purkinje fibers. Evidence for the role of normal automaticity as an underlying cellular mechanism.
Authors: Viamonte V A , Rosen M R
Published: June 2011

Premature escape beats induced in conscious dogs with chronic complete atrioventricular block have been defined as escape beats occurring on cessation of overdrive pacing and having a coupling interval to the last paced beat shorter than the coupling interval between the premature escape beat and the second postpacing beat. Triggered activity has been proposed as the primary underlying mechanism. We used standard microelectrode techniques to study the effects of overdrive pacing on normal automatic canine Purkinje fibers to determine if premature escape beats could be induced and if so, to define the underlying cellular mechanism(s). For this purpose, we overdrive-paced Purkinje fibers for 10 and 50 seconds and for 10 and 50 beats at a pacing cycle length (PCL) of 1,000-200 msec. In addition, to help distinguish among major arrhythmogenic mechanisms, we used a matrix of drugs consisting of propranolol, nadolol, lidocaine, ethmozin, and doxorubicin. Fifty-second stimulation trains induced "classic" overdrive suppression of the first three postpacing impulses, whereas 10-second overdrive pacing induced significant overdrive suppression only at a PCL of 200 msec. With 50-beat overdrive pacing and a PCL of 1,000-600 msec, there was overdrive suppression of postpacing impulses, whereas reduced overdrive suppression was observed at a PCL of 400-200 msec. Ten-beat stimulation trains induced a "flat response" of postpacing impulses. Ten- and 50-beat overdrive pacing provoked premature escape beats in 66% of the fibers, with the higher incidence at a PCL of 200 msec for 50-beat stimulation trains. No shortening of the coupling interval of premature escape beats was observed at faster pacing rates. Only lidocaine (which suppresses normal automaticity) abolished premature escape beats. We conclude that normal automaticity is the most likely mechanism underlying premature escape beats in Purkinje fibers with high levels of membrane potential.
5-year incidence of atherosclerotic vascular disease in relation to general risk factors, insulin level, and abnormalities in lipoprotein composition in non-insulin-dependent diabetic and nondiabetic subjects.
Authors: Uusitupa M I , Niskanen L K , Siitonen O , Voutilainen E , Pyörälä K
Published: June 2011

The 5-year incidence of myocardial infarction and claudication was examined in a group of middle-aged patients (n = 133, 70 men and 63 women) with newly diagnosed non-insulin-dependent diabetes and nondiabetic control subjects (n = 144, 62 men and 82 women). The effects of general risk factors, plasma insulin level, and lipoprotein abnormalities on the incidence of myocardial infarction and claudication were also evaluated by univariate analyses in both diabetic patients and nondiabetic subjects and by multivariate analyses combining both groups. The age-adjusted incidence of myocardial infarction was higher both in diabetic men (19.4%) and diabetic women (11.0%) than in nondiabetic men (3.2%, p = 0.009) and nondiabetic women (3.0%, p = 0.047). Similarly, the age-adjusted incidence of claudication was higher among the diabetic patients (20.3% vs. 8.0% for men, p = 0.06; 21.8% vs. 4.2% for women, p = 0.003). None of the general risk factors (i.e., low density lipoprotein [LDL] cholesterol, blood pressure, smoking, and high density lipoprotein [HDL] cholesterol) showed an association with the risk of myocardial infarction either in the diabetic or nondiabetic groups of subjects, but an ischemic electrocardiographic abnormality at the baseline examination predicted myocardial infarction in diabetic men. In univariate analyses in diabetic subjects, high serum total cholesterol, low HDL cholesterol, high very low density lipoprotein (VLDL) cholesterol, and high total, LDL and VLDL triglycerides, and in nondiabetic subjects, high VLDL cholesterol and LDL triglycerides were associated with the appearance of claudication. In multivariate analyses including both diabetic and control subjects, only diabetes had an independent association with myocardial infarction, whereas smoking, high LDL triglycerides or VLDL cholesterol, and high fasting plasma insulin showed independent relations to claudication. The present results indicate that changes in lipoprotein composition characteristic of non-insulin-dependent diabetes are atherogenic and increase the risk of atherosclerotic vascular disease. Furthermore, high plasma insulin might also be involved in atherogenesis, independent of lipoprotein abnormalities.