bluuebunny/crossref_metadata_2025 huggingface dataset:
Balloon angioplasty for recurrent coarctation of aorta. Immediate and long-term results.
Authors: Hijazi Z M , Fahey J T , Kleinman C S , Hellenbrand W E
Published: June 2012

BACKGROUND

As angioplasty techniques have been refined and larger low-profile balloons developed, a nonsurgical approach to recoarctation has become available. Several reports have documented both the efficacy and safety of this procedure. However, there are little data available on the long-term follow-up of these patients. This report details the initial results and long-term evaluation of both the relief of obstruction and the presence of hypertension after balloon angioplasty for recurrent coarctation.

METHODS AND RESULTS

Balloon angioplasty for recurrent coarctation of the aorta was performed 29 times in 26 patients at a median age of 4 years and 9 months (range, 4 months to 29 years), with eight patients less than 1 year old. Initial surgical techniques were end-to-end anastomosis in 11 patients, subclavian flap aortoplasty in 11 patients, and patch aortoplasty in four patients. Angioplasty was performed at a median interval of 2 years and 7 months (range, 4 months to 23 years) after surgery. Mean peak systolic pressure difference across the coarctation decreased from 40.0 +/- 16.8 to 10.3 +/- 9.5 mm Hg (p less than 0.05) after the initial angioplasty, and mean diameter of the aortic lumen at the coarctation site increased from 5.8 +/- 3.5 to 9.0 +/- 4.3 mm (p less than 0.05). There was no mortality, and only one patient developed an aneurysm (4%). Three patients underwent repeat angioplasty for a pressure difference of more than 20 mm Hg. Long-term follow-up is available on 24 of 26 patients with a mean follow-up of 42 +/- 24 months (range, 12-88 months). Mean peak systolic pressure difference across the area of coarctation decreased from 40.3 +/- 17.4 before angioplasty to 8.5 +/- 8.3 mm Hg after final angioplasty (p less than 0.05) and 7.5 +/- 7.5 mm Hg at follow-up. Mean peak systolic blood pressure in the upper extremities decreased from 133.1 +/- 14.9 before angioplasty to 111.1 +/- 14.1 mm Hg at long-term follow-up (p less than 0.05).

CONCLUSIONS

Balloon angioplasty should be considered the treatment of choice for relief of recurrent aortic coarctation.
Dobutamine increases cardiac output of the total artificial heart. Implications for vascular contribution of inotropic agents to augmented ventricular function.
Authors: Binkley P F , Murray K D , Watson K M , Myerowitz P D , Leier C V
Published: June 2012

BACKGROUND

The synthetic catecholamine dobutamine increases stroke volume in normal subjects and in patients with congestive heart failure. In addition to its direct influence on myocardial contractility, dobutamine may significantly modulate vascular tone because of its alpha- and beta-adrenergic agonist activity.

METHODS AND RESULTS

To test the hypothesis that such vasoactive properties significantly contribute to the improved ventricular performance noted with this agent, hemodynamic parameters were measured during stepped ascension infusion of dobutamine in a model that is insensitive to positive inotropic stimulation. Administration of dobutamine in nine calves that underwent replacement of the native right and left ventricles with pneumatically driven total artificial hearts resulted in a significant (p = 0.0001) increase in cardiac output from 7.0 +/- 1.8 to 8.2 +/- 1.8 l/min and a significant (p = 0.0001) decrease in total peripheral vascular resistance from 1,224 +/- 559 to 745 +/- 317 dyne.sec/cm5. A less marked influence was noted on the pulmonary vasculature, with pulmonary vascular resistance exhibiting a significant (p less than 0.05) decrease from its baseline value only at the peak infusion. Consistent with an increase in venous return, both left and right atrial pressures increased significantly (p less than 0.005) with dobutamine administration.

CONCLUSIONS

These data demonstrate that the vasoactive properties of dobutamine significantly contribute to improved ventricular performance independent of direct myocardial stimulation. This effect appears to result in part from a direct modulation of myocardial stimulation. This effect appears to result in part from a direct modulation of arterial and venous tones rather than from a reflex response to primary changes in contractility.
Interferon-gamma inhibits arterial stenosis after injury.
Authors: Hansson G K , Holm J
Published: June 2012

BACKGROUND

Arterial injury initiates a proliferative response among the smooth muscle cells of the artery. This leads to the formation of a thickened intima that may reduce the diameter of the arterial lumen. Such intimal lesions often develop after vascular surgery and angioplastic procedures. Previous cell culture studies have shown that the lymphokine, interferon-gamma (gIFN), inhibits smooth muscle cell proliferation.

METHODS AND RESULTS

We therefore tested whether administration of exogenous gIFN could inhibit the development of intimal lesions. Rat carotid arteries were denuded with a balloon catheter, resulting in the formation of a standardized intimal lesion. The animals were then treated with recombinant rat gIFN at 200,000 units (approximately 400,000 units or 100 micrograms/kg body wt) administered parenterally once daily for 7 days. Autoradiographic analysis of 3H-thymidine incorporation revealed that gIFN reduced the early smooth muscle replication by approximately 75%. gIFN treatment for 1 week resulted in a 50% reduction of intimal cross-section area at 2 weeks after injury when compared to control rats injected with buffer alone. The difference in lesion development persisted in rats analyzed 10 weeks after injury, suggesting that proliferative events during the first week determine the long-term development of the intima. Inhibition of lesion development was accompanied by expression of the class II histocompatibility (Ia) gene, RT1B, suggesting that both were directly related to the administration of gIFN.

CONCLUSIONS

These results show that gIFN is a potent inhibitor of the formation of arterial proliferative lesions in vivo. It is possible that gIFN could be useful in preventing arterial stenosis after surgery and angioplasty in man.
Loss of flow-mediated endothelium-dependent dilation occurs early in the development of atherosclerosis.
Authors: McLenachan J M , Williams J K , Fish R D , Ganz P , Selwyn A P
Published: June 2012

BACKGROUND

Healthy arteries exhibit endothelium-dependent dilation in response to both local acetylcholine and increased blood flow. In humans, clinically overt coronary artery disease is characterized by loss of dilation to both acetylcholine and blood flow. The temporal relation, however, between functional abnormalities of the endothelium and the development of atherosclerosis has not been established.

METHODS AND RESULTS

We examined endothelial vasodilator function in vivo at an early stage of the development of atherosclerosis. Two groups of seven Macaca fascicularis monkeys were studied; one group was fed a high cholesterol diet (0.73-1.0 mg cholesterol per calorie) for 11 months. Cholesterol feeding was associated with increased plasma cholesterol levels and with intimal thickening of the iliac arteries but with no reduction in luminal diameter. Endothelium-dependent vasomotor responses of the iliac arteries were then examined in vivo by quantitative contrast angiography. Acetylcholine produced significant dilation in the controls but paradoxical constriction in the group with early atherosclerosis (+9.0 +/- 3.2% versus -5.3 +/- 5.4%, p less than 0.05). In response to a twofold increase in blood flow achieved by administering adenosine distal to the arterial segment under examination, the controls again dilated, whereas the atherosclerotic group failed to dilate (+ 11.6 +/- 2.1% versus + 0.5 +/- 2.4%, p less than 0.05). Both groups, however, were able to dilate, and dilated equally, to the nonendothelium-dependent agent nitroglycerin (+ 13.7 +/- 4.8% versus + 19.1 +/- 4.3%, NS).

CONCLUSIONS

Endothelium-dependent vasodilation in response to both acetylcholine and increased blood flow may be lost early in the course of developing atherosclerosis before the appearance of stenosing and occlusive disease.
Neuronal reuptake of norepinephrine and production of dihydroxyphenylglycol by cardiac sympathetic nerves in the anesthetized dog.
Authors: Eisenhofer G , Smolich J J , Cox H S , Esler M D
Published: June 2012

BACKGROUND

Reuptake of norepinephrine by cardiac sympathetic nerves before and during two levels of electrical stimulation of the left ansa subclavia was estimated in anesthetized dogs from the cardiac production of dihydroxyphenylglycol (DHPG), the intraneuronal metabolite of norepinephrine.

METHODS AND RESULTS

The method depended on the effects of neuronal uptake blockade with desipramine on the cardiac production of [3H]DHPG from intravenously infused [3H]norepinephrine. The ratio of the desipramine-induced decrease in the cardiac extraction of [3H]norepinephrine to the production of [3H]DHPG was used to transform the cardiac production of DHPG from recaptured norepinephrine into a rate for norepinephrine reuptake. Cardiac spillover of norepinephrine into plasma increased from 49 +/- 12 to 205 +/- 40 and 451 +/- 118 pmol/min during sympathetic activation. Cardiac DHPG production increased from 108 +/- 18 to 166 +/- 34 and 240 +/- 47 pmol/min. Desipramine decreased resting cardiac DHPG production by 20% and completely blocked the stimulation-induced increase. Thus, most (80%) cardiac DHPG produced at rest was derived from norepinephrine leaking from storage vesicles. This amount remained constant, and that derived from recaptured norepinephrine increased during sympathetic activation. The cardiac extraction of [3H]norepinephrine (126,000 dpm/min) and production of [3H]DHPG (3,790 dpm/min) were decreased by 55-57% after desipramine. Thus, only 3% of the norepinephrine recaptured by cardiac sympathetic nerves appeared in plasma as DHPG. The remainder was sequestered into storage vesicles (more than 94%) or ultimately formed metabolites other than DHPG (less than 3%). Reuptake of norepinephrine by cardiac sympathetic nerves was 1,188 +/- 476 pmol/min and increased in parallel with cardiac norepinephrine spillover to 4,182 +/- 1,982 and 6,594 +/- 2,241 pmol/min during sympathetic stimulation.

CONCLUSIONS

Of the norepinephrine released by cardiac sympathetic nerves, 16-fold more was recaptured than entered plasma. Combined estimation of norepinephrine reuptake and spillover offers an approach to assess the efficiency of neuronal reuptake in disorders of cardiac function.
Atrial contribution to ventricular filling in mitral stenosis.
Authors: Meisner J S , Keren G , Pajaro O E , Mani A , Strom J A , Frater R W , Laniado S , Yellin E L
Published: June 2012

BACKGROUND

The importance of the contribution of atrial systole to ventricular filling in mitral stenosis is controversial. The cause of reduced cardiac output following the onset of atrial fibrillation may be due to an increased heart rate, a loss of booster pump function, or both.

METHODS AND RESULTS

We studied the atrial contribution to filling under a variety of conditions by combining noninvasive studies of patients with computer modeling. Thirty patients in sinus rhythm with mild-to-severe stenosis were studied with two-dimensional and Doppler echocardiography for measurement of mitral flow velocity and mitral valve area (MVA). The mean +/- SD atrial contribution to left ventricular filling volume was 18 +/- 10% and varied inversely with mitral resistance. Patients with mild mitral stenosis (MVA, 1.8 +/- 0.7 cm2) and severe mitral stenosis (MVA, 0.9 +/- 0.2 cm2) had atrial contributions of 29 +/- 4% and 9 +/- 5%, respectively. The pathophysiological mechanisms responsible for these trends were further investigated by the computer model. In modeled severe mitral stenosis, increasing heart rate from 75 to 150 beats/min caused an increase of 5.2 mm Hg in mean left atrial pressure, whereas loss of atrial contraction at a heart rate of 150 beats/min caused only a 1.3 mm Hg increase.

CONCLUSIONS

The atrial booster pump contributes less to ventricular filling in mitral stenosis than in the normal heart, and the loss of atrial pump function is less important than the effect of increasing heart rate as the cause of decompensation during atrial fibrillation.
Polymorphous ventricular tachycardia associated with acute myocardial infarction.
Authors: Wolfe C L , Nibley C , Bhandari A , Chatterjee K , Scheinman M
Published: June 2012

BACKGROUND

During a 2.9-year period, 11 patients developed polymorphous ventricular tachycardia 1-13 days after acute anterior (seven patients) or inferior (four patients) myocardial infarction. None of the 11 patients had sinus bradycardia (mean heart rate, 90 +/- 23 beats/min), but three had a sinus pause immediately before the onset of polymorphous ventricular tachycardia. In all 11 patients, the QT interval and corrected QT interval (QTc) were normal or minimally prolonged (QT, 385 +/- 34 msec; QTc, 442 +/- 40 msec). None had significant hypokalemia (mean serum potassium concentration, 4.3 +/- 0.5 meq/l) or a grossly abnormal serum magnesium or calcium concentration (2.1 +/- 0.4 and 8.9 +/- 0.7 mg/dl, respectively).

METHODS AND RESULTS

Immediately before the onset of polymorphous ventricular tachycardia, symptoms and/or electrocardiographic changes consistent with recurrent myocardial ischemia occurred in nine of 11 patients. One patient died before drug therapy could be initiated. Lidocaine was used in 10 patients and proved to be effective in only one. Intravenous procainamide was used in six patients: one improved, and five had recurrence of polymorphous ventricular tachycardia. Bretylium was used in five patients and was ineffective in all cases. Overdrive pacing was used in four patients and failed to suppress recurrent arrhythmias in all cases. Four patients with persistent polymorphous ventricular tachycardia unresponsive to lidocaine, procainamide, or bretylium responded to intravenous amiodarone. One patient with polymorphous ventricular tachycardia that was consistently preceded by ST segment elevation responded to intravenous nitroglycerin. Two patients with persistent polymorphous ventricular tachycardia and obvious recurrent ischemia unresponsive to pharmacological intervention responded to emergency coronary revascularization. A third patient who experienced recurrent angina and polymorphous tachycardia was initially stabilized with pharmacological therapy but subsequently underwent elective revascularization and has remained stable without antiarrhythmic therapy.

CONCLUSIONS

Post-myocardial infarction polymorphous ventricular tachycardia is not consistently related to an abnormally long QT interval, sinus bradycardia, preceding sinus pauses, or electrolyte abnormalities. This arrhythmia has a variable response to class I antiarrhythmics but may be suppressed by intravenous amiodarone therapy. It is often associated with signs or symptoms of recurrent myocardial ischemia. Furthermore, coronary revascularization appears to be effective in preventing the recurrence of polymorphous ventricular tachycardia when associated with recurrent postinfarction angina.
Effects of myocardial alpha 1-adrenergic receptor stimulation and blockade on contractility in humans.
Authors: Landzberg J S , Parker J D , Gauthier D F , Colucci W S
Published: June 2012

BACKGROUND

Although alpha-adrenergic receptors are present in both normal and failing human left ventricular myocardium and mediate a positive inotropic effect in several other species, it is not known whether stimulation of myocardial alpha-adrenergic receptors exerts a positive inotropic effect or contributes to basal contractile state in vivo in humans.

METHODS AND RESULTS

We studied 15 patients with angiographically normal coronary arteries (seven with normal left ventricular function and eight with left ventricular failure). To avoid the confounding effects of changes in ventricular loading conditions and systemic reflex mechanisms, the alpha-adrenergic receptor-selective antagonist phentolamine and agonist phenylephrine were infused directly into the left main coronary artery, and the change in contractile state was assessed by measuring left ventricular peak (+)dP/dt. Phentolamine alone had no effect on left ventricular contractility. Phenylephrine exerted a concentration-related positive inotropic effect in patients with normal as well as those with failing ventricles. The alpha-adrenergic effect of phenylephrine, defined as the component blocked by phentolamine, was significantly less in patients with ventricular failure (108 +/- 28 mm Hg/sec) than in normal subjects (248 +/- 54 mm Hg/sec; p less than 0.03).

CONCLUSIONS

Myocardial alpha-adrenergic receptors do not contribute to the maintenance of basal left ventricular contractile state in humans. However, stimulation of myocardial alpha-adrenergic receptors exerts a positive inotropic effect, the magnitude of which may be attenuated in patients with heart failure.
Relative risk analysis of angiographic predictors of restenosis within the coronary Wallstent.
Authors: Strauss B H , Serruys P W , de Scheerder I K , Tijssen J G , Bertrand M E , Puel J , Meier B , Kaufmann U , Stauffer J C , Rickards A F
Published: June 2012

BACKGROUND

Late angiographic narrowing has been observed following coronary implantation of the Wallstent. To identify the angiographic variables that predict restenosis within the stented segment, a retrospective study of data from the European Wallstent core laboratory was performed.

METHODS AND RESULTS

Follow-up angiograms (excluding patients with in-hospital occlusions) were analyzed for 214 lesions in 176 patients (78% restudy rate). The incidence of restenosis within the stented segment was 35% by lesion and 35% by patient for criterion 1 (greater than or equal to 0.72 mm loss in minimal luminal diameter) and 24% by lesion and 24% by patient for criterion 2 (diameter stenosis greater than or equal to 50% at follow-up). The association between 16 variables and restenosis was determined by a relative risk ratio assessment. Variables with significant risk ratios for restenosis with criterion 1 were use of multiple stents/lesion (relative risk, 1.56; 95% confidence interval [CI], 1.08-2.25) and oversized (unconstrained stent diameter exceeding reference diameter greater than 0.7 mm) stents (relative risk, 1.64; 95% CI, 1.10-2.45), and for criterion 2, oversizing by more than 0.70 mm (relative risk, 1.93; 95% CI, 1.13-3.31), bypass grafts (relative risk, 1.62; 95% CI, 0.98-2.66), use of multiple stents/lesion (relative risk, 1.61; 95% CI, 0.97-2.67) and residual diameter stenosis more than 20% post stenting (relative risk, 1.51; 95% CI, 0.91-2.50).

CONCLUSIONS

It is concluded that several angiographic variables are significantly associated with late angiographic narrowing after stenting in the coronary arteries. We suggest that stent operators avoid excessive oversizing in the selection of stent diameter and the use of multiple stents per lesion to lessen the risk of late restenosis.
Modulation of drug effects by regional sympathetic denervation and supersensitivity.
Authors: Stanton M S , Zipes D P
Published: June 2012

BACKGROUND

Regional sympathetic denervation, such as that produced by a myocardial infarction, causes electrophysiological heterogeneity in the ventricles. The purpose of this study was to test the hypothesis that such denervation could cause drugs to exert heterogeneous myocardial effects.

METHODS AND RESULTS

Sympathetic stimulation increases the amplitude of cesium chloride-induced early afterdepolarizations (EADs). The amplitude of these induced EADs was used to determine whether drug responses were different in innervated versus denervated areas of the heart. A canine model of sympathetic denervation was created at the cardiac apex by either transmural myocardial infarction (n = 19) or phenol application (n = 11). Cesium chloride (84 mg/kg) was infused while monophasic action potential recordings were simultaneously obtained from the base and apex of the left ventricle using an epicardial contact electrode. We found that control (innervated) dogs (n = 17) showed no difference in the EAD amplitude recorded from the apex compared with the base. In dogs with apical sympathetic denervation, the EAD amplitude was greater at the innervated base during ansae subclaviae stimulation than at the denervated apex (25.8 +/- 6.6% at base versus 18.8 +/- 6.7% at apex, p less than 0.001). However, during norepinephrine infusion, the EADs recorded from the denervated apex were greater than those recorded from the innervated base (23.3 +/- 7.6% at apex versus 20.6 +/- 6.0% at base, p less than 0.02) due to denervation supersensitivity.

CONCLUSIONS

These data show that regional myocardial denervation creates autonomic and electrophysiological heterogeneity and the substrate for heterogeneous drug actions. This drug-induced electrophysiological heterogeneity may be another mechanism for proarrhythmia.
Influx of neutrophils into the walls of large epicardial coronary arteries in response to ischemia/reperfusion.
Authors: Kloner R A , Giacomelli F , Alker K J , Hale S L , Matthews R , Bellows S
Published: June 2012

BACKGROUND

There are several clinical situations in which large epicardial coronary arteries are deprived of blood flow, such as occurs when an obstructing thrombus or embolus lodges within a vessel or during coronary dissection. There is little information concerning the effect of flow deprivation on large epicardial coronary arteries.

METHODS AND RESULTS

We studied a model in which a segment of a large epicardial coronary artery was deprived of blood flow using both proximal and distal clamps for 3 hours followed by reperfusion. On examination by light microscopy of cross sections of the arteries, 19 +/- 6 neutrophils were present in the intima of ischemic/reperfused vessels, whereas only a mean of 4 +/- 3 (SEM) were present in the intima of nonischemic vessels (p less than 0.02). On average, there were 17 +/- 9 neutrophils just under the elastic lamina in ischemic/reperfused vessels versus none in the nonischemic vessels (p less than 0.05); there were 16 +/- 10 neutrophils present within the media of ischemic/reperfused vessels, and none (p less than 0.05) in the nonischemic vessels. Electron microscopic analysis revealed that neutrophils in the ischemic/reperfused vessels were often "sandwiched" between the endothelial cells and the elastic lamina. Ultrastructural abnormalities within the myocardium also revealed damage to the microvasculature, including the presence of neutrophils within the vessels and erythrocyte stasis. To rule out the possibility that findings in the large epicardial arteries were due to toxic substances from static blood within the isolated arterial segment, a protocol was performed in which blood was removed from the isolated segment. Again, neutrophil infiltration into the vessel was observed. Resting mean epicardial coronary artery blood flow before coronary occlusion was 19 +/- 3 ml/min; mean coronary blood flow 2.5 hours after reperfusion was identical at 19 +/- 3 ml/min. Response to both endothelial-dependent vasodilation (acetylcholine) and endothelial-independent vasodilation (nitroglycerin) challenges was normal early after reperfusion but was depressed late after reperfusion, suggesting progressive vascular dysfunction and hence a form of vascular reperfusion injury in this model.

CONCLUSIONS

When large epicardial coronary arteries are deprived of blood flow, followed by reperfusion in this model, neutrophils migrate into the vessel wall as well as into the microvasculature. These abnormalities are associated with reduced endothelial-dependent and endothelial-independent coronary vasodilator reserve.
Early afterdepolarizations induced by isoproterenol in patients with congenital long QT syndrome.
Authors: Shimizu W , Ohe T , Kurita T , Takaki H , Aihara N , Kamakura S , Matsuhisa M , Shimomura K
Published: June 2012

BACKGROUND

Several recent experimental and clinical studies have shown that early afterdepolarizations (EADs) are important in the genesis of QTU prolongation and ventricular tachyarrhythmias (VTs) in patients with long QT syndrome. On the other hand, sympathetic stimulation is well known to contribute to the genesis of QTU prolongation and VTs in patients with congenital long QT syndrome. The present study was performed to examine the influence of isoproterenol on the genesis of EADs and on the action potential durations and QTU intervals in patients with congenital long QT syndrome.

METHODS AND RESULTS

We recorded monophasic action potentials (MAPs) with a contact electrode during right atrial pacing at a constant cycle length of 500 msec before and after continuous isoproterenol infusion (1 microgram/min). MAPs were obtained from the right and left ventricular endocardium in six patients with congenital long QT syndrome (LQT group, 18 recording sites) and in eight control patients (control group, 19 recording sites). Although no EADs were recorded from either group during the control state, MAP duration at 90% repolarization (MAPD90) was significantly longer in the LQT group (n = 18) than in the control group (n = 19) (275 +/- 36 versus 231 +/- 22 msec; p less than 0.0005). Isoproterenol induced EADs in four of the six LQT patients (five of 18 recording sites) but not in the eight control patients (zero of 19 recording sites). The appearance of EADs in the LQT group was associated with an increased amplitude of the late component of the TU complex, and the corrected QT (QTc) interval was prolonged by isoproterenol from 543 +/- 53 to 600 +/- 30 msec 1/2 (n = 6; p less than 0.05). Isoproterenol also prolonged the MAPD90 from 275 +/- 36 to 304 +/- 50 msec in the LQT group (n = 18; p less than 0.005), whereas it shortened the MAPD90 from 231 +/- 22 to 224 +/- 25 msec in the control group (n = 19; p less than 0.05). Moreover, isoproterenol increased the dispersion of MAPD90 (difference between the longest MAPD90 and the shortest MAPD90 in each patient) from 30 +/- 5 to 62 +/- 35 msec in the LQT group (n = 6; p = 0.08), whereas it did not change the dispersion of MAPD90 in the control group (n = 8; 25 +/- 14 versus 27 +/- 14 msec).

CONCLUSIONS

These results suggest that patients with congenital long QT syndrome have primary repolarization abnormalities and that EADs induced by isoproterenol play an important role in the exaggeration of these repolarization abnormalities.
Saturated fat intake and insulin resistance in men with coronary artery disease. The Stanford Coronary Risk Intervention Project Investigators and Staff.
Authors: Maron D J , Fair J M , Haskell W L
Published: June 2012

BACKGROUND

To determine whether there is an association between diet and plasma insulin concentration that is independent of obesity, we studied the relation of dietary composition and caloric intake to obesity and plasma insulin concentrations in 215 nondiabetic men aged 32-74 years with angiographically proven coronary artery disease.

METHODS AND RESULTS

After adjusting for age, the intake of saturated fatty acids and cholesterol were positively correlated (p less than 0.05) with body mass index (r = 0.18, r = 0.16), waist-to-hip circumference ratio (r = 0.21, r = 0.22), and fasting insulin (r = 0.26, r = 0.23). Carbohydrate intake was negatively correlated with body mass index (r = -0.21), waist-to-hip ratio (r = -0.21), and fasting insulin (r = -0.16). Intake of monounsaturated fatty acids did not correlate significantly with body mass index or waist-to-hip circumference ratio but did correlate positively with fasting insulin (r = 0.24). Intake of dietary calories was negatively correlated with body mass index (r = -0.15). In multivariate analysis, intake of saturated fatty acids was significantly related to elevated fasting insulin concentration independently of body mass index.

CONCLUSIONS

These cross-sectional findings in nondiabetic men with coronary artery disease suggest that increased consumption of saturated fatty acids is associated independently with higher fasting insulin concentrations.
Pulmonary ventilation/perfusion defects induced by epinephrine during cardiopulmonary resuscitation.
Authors: Tang W , Weil M H , Gazmuri R J , Sun S , Duggal C , Bisera J
Published: June 2012

BACKGROUND

Epinephrine has been shown to impair pulmonary excretion of CO2 during resuscitation. This phenomenon was investigated in a rodent model of cardiac arrest and conventional resuscitation.

METHODS AND RESULTS

The effects of racemic epinephrine were compared with the selective alpha 1-agonist methoxamine and with saline placebo during cardiac resuscitation in 15 Sprague-Dawley rats mechanically ventilated with gas containing 70% oxygen. Epinephrine and methoxamine but not saline placebo significantly increased coronary perfusion pressure from approximately 32 to 55 mm Hg. Following epinephrine, end-tidal PCO2 decreased from approximately 10 to 5 mm Hg. This was associated with a time-coincident decrease in PaO2 from approximately 130 to 74 mm Hg and an increase in PaCO2 from approximately 26 to 40 mm Hg. These changes indicated increases in alveolar dead space ventilation concomitant with increases in pulmonary arteriovenous admixture. No such effects were observed after administration of either methoxamine or saline placebo. Each of the 15 rats was successfully resuscitated. However, a significantly larger number of transthoracic countershocks were required after epinephrine compared with methoxamine or placebo before return of spontaneous circulation.

CONCLUSIONS

Epinephrine induced ventilation/perfusion during cardiopulmonary resuscitation as a result of redistribution of pulmonary blood flow.
Transcatheter occlusion of the persistently patent ductus arteriosus. Forty-month follow-up and prevalence of residual shunting.
Authors: Hosking M C , Benson L N , Musewe N , Dyck J D , Freedom R M
Published: June 2012

BACKGROUND

Percutaneous closure of the persistently patent ductus arteriosus with the Rashkind prosthesis is an established effective therapeutic modality, although some patients are left with residual shunting. To evaluate this, a retrospective study of the prevalence of persistent shunting over a 40-month period in the first 190 patients was undertaken.

METHODS AND RESULTS

All patients (male 45, female 145; mean age, 3.9 +/- 3.6 years; range, 5 months to 20 years) had serial clinical and color-flow echocardiographic follow-up at 6-12-month intervals (range, 6-40 months). Four patients required surgical removal of an embolized device, leaving a cohort of 186 patients in whom 196 procedures were performed, resulting in successful placement of 195 devices (43 17-mm [22%] and 152 12-mm [78%]). Complications occurred in seven of 195 procedures (3.6%). Nine of 10 attempted reocclusions (all with 12-mm devices) were successful. The prevalence of residual shunting was 38% at 1 year, 18% at 2 years, and 8% at 40 months. Patients with ductus measuring less than 4 mm had a higher success of initial occlusion. Thirty-four patients were left with residual shunting determined by color-flow Doppler study, but no anatomic or echocardiographic features were found predictive for residual shunting. All remain asymptomatic with 26 (76%) having no detectable murmur, two (6%) a continuous murmur, and six (18%) a systolic murmur.

CONCLUSIONS

Catheter occlusion will obviate the need for surgery in the majority of patients presenting with persistently patent ductus arteriosus. Reocclusion has been found feasible in those with continuous murmurs (nine of nine) and should be offered early because it is unlikely for spontaneous closure to occur in this group. It appears prudent to follow those with small residual shunting because further spontaneous closure can occur.
Use of radiofrequency current to ablate accessory connections in children.
Authors: Dick M , O'Connor B K , Serwer G A , LeRoy S , Armstrong B
Published: June 2012

BACKGROUND

Several investigators have recently ablated electrophysiologically mapped accessory connections in the adult human myocardium by using radiofrequency current. To examine the effectiveness and safety of radiofrequency current for ablation of accessory connections in children, 20 consecutive patients (age, 3-18 years) with preexcitation and/or supraventricular tachycardia were evaluated by electrophysiological study.

METHODS AND RESULTS

Nineteen of the 20 patients were completely studied and demonstrated accessory connections. After identification of the earliest retrograde atrial activation site, a steerable 7F catheter (with a 4-mm-long electrode at the distal tip) was placed within the ventricular cavity ipsilateral to the accessory connection and positioned at the atrioventricular valve annulus directly opposite the earliest point of retrograde atrial activation. Radiofrequency current was delivered at 50-65 volts for 10-60 seconds at a frequency of 500 kHz. Radiofrequency pulses were delivered for two to 26 trials. Upon completion of radiofrequency trials, repeat electrophysiological testing was performed. Thirteen of 19 subjects (68%) experienced definite successful ablation of their accessory pathway; an additional patient had probable successful ablation, yielding an overall success rate of 74%. Eighty-seven percent of individuals with a left-sided pathway had permanent ablation and 100% with a manifest left-sided pathway experienced successful ablation. Only 29% of the first seven patients had a successful result; in contrast, 92% of the next 12 patients had successful interruption of their accessory pathways. After ablation, 4-day continuous electrocardiographic telemetry disclosed no significant arrhythmias. CPK enzyme rises peaked at 12-24 hours. The rise was excessive and associated with general anesthesia in five patients. The isoenzyme MB fraction rose mildly in five other patients and returned to normal within 72 hours. No clinical or electrocardiographic evidence of myocardial ischemia was detected. Follow-up for 4-12 months indicates no return of preexcitation or tachycardia in any patient whose accessory connection was successfully ablated.

CONCLUSIONS

This experience indicates that radiofrequency current is an effective and safe technique for ablation of accessory connections in children.
Counter-regulatory responses to continuous and intermittent therapy with nitroglycerin.
Authors: Parker J D , Farrell B , Fenton T , Cohanim M , Parker J O
Published: June 2012

BACKGROUND

Vasodilator therapy may be associated with reflex counter-regulatory responses, and these responses may play a role in the development of tolerance to nitroglycerin (GTN).

METHODS AND RESULTS

Standing systolic blood pressure, body weight, urinary sodium, and hormonal responses to continuous (n = 10) and intermittent (n = 10) transdermal GTN administration were studied in normal volunteers. There was rapid attenuation of the hypotensive response to transdermal GTN therapy in the continuous but not in the intermittent therapy group. Significant weight gain and sodium retention occurred during continuous but not during intermittent GTN therapy. This was accompanied by a greater decrease in hematocrit in the continuous group, a finding that suggests that plasma volume expansion occurred during continuous GTN therapy. Continuous GTN therapy was associated with increases in plasma norepinephrine, atrial natriuretic peptide, arginine, vasopressin, and plasma renin activity. A different pattern of neurohormonal response was seen during intermittent therapy, with values tending to return to baseline levels after the nitrate-free interval.

CONCLUSIONS

Continuous transdermal GTN therapy leads to counter-regulatory responses associated with sodium retention and probable plasma volume expansion. By contrast, intermittent transdermal GTN therapy is associated with a different pattern of hormonal response, the lack of sodium retention and no evidence of plasma volume expansion. It is likely that these counter-regulatory responses play an important role in the attenuation of nitrate effects.
Large artery function in patients with chronic heart failure. Studies of brachial artery diameter and hemodynamics.
Authors: Arnold J M , Marchiori G E , Imrie J R , Burton G L , Pflugfelder P W , Kostuk W J
Published: June 2012

BACKGROUND

Although progressive chronic congestive heart failure (CHF) is associated with elevated systemic vascular resistance and increased impedance to ventricular outflow, the contribution of changes in large artery function has not been well documented in humans.

METHODS AND RESULTS

We studied 45 patients with a broad range of clinical severity of CHF and compared noninvasive measurements of brachial artery diameter, flow, and pulse wave velocity with 22 normal controls of similar age. In CHF, mean arterial pressure was lower than in controls (85 +/- 1 versus 93 +/- 2 mm Hg, p less than 0.001), as were brachial artery diameter (4.07 +/- 0.10 versus 4.53 +/- 0.09 mm, p less than 0.001), flow (40.9 +/- 4.1 versus 70.9 +/- 11.5 ml.min-1, p less than 0.02), compliance (1.29 +/- 0.12 versus 2.00 +/- 0.18 cm4.dyne-1.10(-7), p less than 0.002), and conductance (0.49 +/- 0.05 versus 0.76 +/- 0.13 units, p = 0.06). Limb vascular resistance (40.2 +/- 5.0 versus 20.5 +/- 3.1 units, p less than 0.001) and pulse wave velocity (10.6 +/- 0.5 versus 9.2 +/- 0.4 m.sec-1, p less than 0.03) were higher than in controls. Brachial artery diameter was progressively lower than in controls as severity of CHF increased (New York Heart Association class II, 4.47 +/- 0.23 mm, p = NS; class III, 4.05 +/- 0.10 mm, p less than 0.05; class IV, 3.71 +/- 0.28 mm, p less than 0.05). Similar changes were observed for arterial compliance (class II, 1.76 +/- 0.32 cm4.dyne-1.10(-7), p = NS; class III, 1.21 +/- 0.13 cm4.dyne-1.10(-7), p less than 0.05; class IV, 0.95 +/- 0.10 cm4.dyne-1.10(-7), p less than 0.05). While the lower arterial pressure and flow might be expected to passively reduce arterial diameter, this would be associated with a reduced pulse wave velocity and improved arterial compliance, yet the opposite was observed. Differences in large artery function were not likely caused by underlying atherosclerosis alone, because patients with dilated cardiomyopathy and patients with ischemic heart disease of the same sex, age, left ventricular ejection fraction, and exercise treadmill duration had similar changes in large artery function.

CONCLUSIONS

We conclude that alterations in brachial artery function are present in patients with moderate and severe CHF. The observed reduction in arterial compliance, if present diffusely throughout the arterial tree, could increase left ventricular end-systolic stress directly and through increased velocity of reflected pressure waves from the periphery.
A monoclonal antibody against the platelet glycoprotein IIb/IIIa receptor complex prevents platelet aggregation and thrombosis in a canine model of coronary angioplasty.
Authors: Bates E R , McGillem M J , Mickelson J K , Pitt B , Mancini G B
Published: June 2012

BACKGROUND

The comparative effects of aspirin and F(ab')2 fragments of monoclonal antibody 7E3 against the platelet glycoprotein IIb/IIIa receptor on ex vivo platelet aggregation and in vivo thrombosis were studied in a canine coronary balloon angioplasty model.

METHODS AND RESULTS

Three groups were studied. Group 1 (n = 8) was pretreated with saline placebo, group 2 (n = 8) was pretreated with 325 mg aspirin, and group 3 (n = 8) was pretreated with 0.8 mg/kg 7E3 F(ab')2. Coronary angioplasty was performed in the left anterior descending coronary artery of open-chest dogs under fluoroscopic control; serial measurements of basal and hyperemic coronary blood flows were then made for 2 hours after application of an external stenosis that decreased hyperemic flow by 50%. There were no significant differences in platelet counts or hemodynamic measurements during the experiments. Platelet aggregation was decreased by treatment: group 1, 64 +/- 13% versus 50 +/- 13% (p = NS); group 2, 57 +/- 4% versus 25 +/- 4% (p less than 0.001); and group 3, 77 +/- 5% versus 10 +/- 6% (p less than 0.0002). Compared with initial measurements, the 7E3 antibody was superior to aspirin in maintaining hyperemic coronary blood flow after release of the external stenosis: group 1, 177 +/- 14 versus 21 +/- 14 ml/min (p less than 0.0003); group 2, 189 +/- 9 versus 110 +/- 28 ml/min (p less than 0.008); and group 3, 194 +/- 12 versus 181 +/- 15 ml/min (p less than 0.02). In group 1, arterial occlusion developed in five dogs, and nonocclusive thrombus was seen in three dogs. In group 2, arterial occlusion developed in one dog, and nonocclusive thrombus was seen in five dogs. No thrombotic material was visualized in group 3 dogs treated with 7E3 F(ab')2.

CONCLUSIONS

In this animal model, the 7E3 antiplatelet antibody is superior to aspirin in inhibiting platelet aggregation, thrombosis, and acute closure after deep arterial injury caused by coronary balloon angioplasty.
Thrombolytic therapy causes an increase in vascular permeability that is reversed by 1-deamino-8-D-vasopressin.
Authors: Rudd M A , Johnstone M T , Rabbani L E , George D , Ware J A , Loscalzo J
Published: June 2012

BACKGROUND

To examine the effect of plasminogen activator therapy on vascular permeability, we used a modified rabbit mesenteric model of extravascular tissue accumulation of radiolabeled albumin.

METHODS AND RESULTS

Albumin deposition was measured after saline, tissue-type plasminogen activator (t-PA; 0.86 mg/kg for 1 hour followed by 0.29 mg/kg for 2 hours), or t-PA plus 1-deamino-8-D-arginine vasopressin (DDAVP; 0.6 mg/kg/hr for 30 minutes) infusion in animals with or without aspirin (ASA; 15-mg/kg bolus) pretreatment. In animals not given ASA, t-PA caused a 240% increase in tissue [125I]albumin accumulation over time (p less than 0.001). DDAVP prevented the rise in albumin accumulation normally seen with t-PA alone (p less than 0.05) in animals not given ASA. In animals pretreated with ASA, t-PA similarly caused an increase in tissue albumin accumulation, but this was significantly attenuated from that of animals not given ASA (p less than 0.03). Interestingly, DDAVP failed to block the response to t-PA in the animals given ASA. Because increases in vascular permeability correlated with increases in bleeding time (r = 0.37, p less than 0.03), these data suggest that the effect of plasmin generation on vascular permeability may contribute to the bleeding tendency seen with thrombolytic therapy. The ability of DDAVP to reverse the bleeding tendency and bleeding time may be due in part to its reversal of the increased vascular permeability induced by the administration of plasminogen activators.

CONCLUSIONS

These data show that plasminogen activation causes an increase in vascular permeability that is inhibited by DDAVP; ASA blunts this action of t-PA and prevents the DDAVP blockade of the increase in permeability induced by t-PA in this rabbit model.
Outcome and assessment after the modified Fontan procedure for hypoplastic left heart syndrome.
Authors: Farrell P E , Chang A C , Murdison K A , Baffa J M , Norwood W I , Murphy J D
Published: June 2012

BACKGROUND

We reviewed the outcome of 76 consecutive patients (age range, 5 months to 6 years; median age, 19 months) who underwent a modified Fontan procedure after initial palliative surgery for hypoplastic left heart syndrome (HLHS) between January 1984 and December 1989.

METHODS AND RESULTS

Modifications of the Fontan procedure included transatrial baffle of pulmonary venous return to the tricuspid valve (n = 10) or inferior vena cava baffle within the right atrium to the superior vena caval-pulmonary artery anastomosis, with pulmonary artery augmentation (n = 66). Actuarial survival rates were 74% (1 month), 58% (12 months), 56% (2 years), and 52% (4 years). Of the 43 survivors, 25 patients have returned for postoperative cardiac catheterization at a medium of 13 months after the Fontan procedure. Mean +/- SD hemodynamic values were cardiac index, 2.8 +/- 0.6 l/min/m2; right arterial pressure, 11 +/- 2 mm Hg; pulmonary artery wedge pressure, 6 +/- 3 mm Hg; and arterial oxygen saturation, 94 +/- 3%. No patient had significant tricuspid or native pulmonary valve insufficiency.

CONCLUSIONS

Survival after the Fontan procedure in patients with HLHS is comparable to survival after a Fontan procedure in patients with other complex congenital heart lesions. In the subgroup of patients with HLHS who survived both reconstructive surgery and a Fontan procedure and have been evaluated by cardiac catheterization after a Fontan procedure, the use of the right ventricle as the systemic ventricle yielded excellent intermediate results for Fontan physiology.
Effect of valve deformity on results and mitral regurgitation after Inoue balloon commissurotomy.
Authors: Feldman T , Carroll J D , Isner J M , Chisholm R J , Holmes D R , Massumi A , Pichard A D , Herrmann H C , Stertzer S H , O'Neill W W
Published: June 2012

BACKGROUND

The effect of valve deformity and patient age adversely affect the results of percutaneous transvenous mitral commissurotomy (PTMC) with conventional balloons.

METHODS AND RESULTS

These factors were characterized after PTMC with the Inoue balloon. The increases in mitral valve area and mitral regurgitation after the procedure were evaluated comparing echocardiographic score of 8 or less versus more than 8, age of less than 60 versus age of 60 years or more, and age of less than 70 versus age of 70 years or more. One hundred sixty-two patients (mean age, 52 +/- 14 years) were studied. For the entire group, mitral valve area increased from 1.0 to 1.8 cm2 (p less than 0.001). Valve area increased from 1.0 +/- 0.3 to 1.8 +/- 0.6 cm2 in patients with echocardiographic score of 8 or less (n = 102) and from 1.0 +/- 0.3 to 1.7 +/- 0.5 cm2 with echocardiographic score of more than 8 (n = 44). Patients less than 60 years old (n = 104) had increases in valve area from 1.0 +/- 0.3 to 1.8 +/- 0.6 cm2 versus 1.0 +/- 0.4 to 1.8 +/- 0.6 cm2 for those 60 years old or older (n = 50) (p = NS). There was no significant difference in resultant valve area when the age division was increased to less than 70 versus 70 years or more. Similarly, the percentage of patients with 2+ or greater increase in mitral regurgitation was not different for those with higher than for those with lower echocardiographic scores (4% versus 12%, p = NS), age of less than 60 versus age of 60 years or more (10% versus 10%, p = NS), or age of less than 70 versus age of 70 or more years (9% versus 18%, p = NS). Valve replacement for mitral regurgitation was performed in four patients (one emergency), all with echocardiographic scores of less than 8.

CONCLUSIONS

Age and extent of valve deformity do not have significant effects on acute results of PTMC using the Inoue balloon. Unique balloon geometry or the controlled, stepwise balloon sizing may explain these acceptable acute results in patients with more-deformed valves.