bluuebunny/crossref_metadata_2025 huggingface dataset:
Effect of dietary potassium on blood pressure, renal function, muscle sympathetic nerve activity, and forearm vascular resistance and flow in normotensive and borderline hypertensive humans.
Authors: Lawton W J , Fitz A E , Anderson E A , Sinkey C A , Coleman R A
Published: June 2011

We evaluated the effect of a low potassium diet on blood pressure in normotensive (NT) and in borderline hypertensive subjects (BHT). There were 11 BHT men (age, 24.6 +/- 1.2 years) and 10 NT men (age, 23.5 +/- 1.0 years). Subjects were studied while on both low potassium, high sodium (30 meq/day, 400 meq/day) diets and high potassium, high sodium (100 meq/day, 400 meq/day) diets, each taken for 6 days. During the low potassium diet, daytime ambulatory systolic blood pressure increased in both NT (123 +/- 5 mm Hg, low potassium, vs. 116 +/- 4 mm Hg, high potassium, p less than 0.01) and BHT groups (134 +/- 3, low potassium, vs. 124 +/- 3, high potassium, p less than 0.001). Mean blood pressure was not different in NT during the two diets but was significantly higher during the low potassium diet in BHT subjects (97 +/- 2 mm Hg low potassium, vs. 92 +/- 1 mm Hg, high potassium, p less than 0.05) without change in heart rate in BHT subjects during the two diets. Low potassium diet increased the postural rise in diastolic blood pressure when subjects changed from the supine position to quiet standing (standing diastolic blood pressure for NT: low potassium, 79 +/- 2 mm Hg vs. high potassium, 72 +/- 2 mm Hg; for BHT: low potassium, 89 +/- 2 mm Hg vs. high potassium diet, 83 +/- 2 mm Hg, p less than 0.01). The effects of low potassium diet on blood pressure were not related to marked changes in renal hemodynamics, in plasma renin activity, in aldosterone, or in norepinephrine, nor to increases in forearm vascular resistance or in muscle sympathetic nerve activity. In fact, muscle sympathetic nerve activity decreased in the BHT group during low potassium compared with high potassium diets (p less than 0.001) and did not change in the NT group. Sympathetic nerve activity was also higher in BHT compared with the NT group during high potassium and low potassium diets, p less than 0.001. In the NT group, the low potassium diet was associated with lower hematocrit levels, weight gain, and increased 24 hour urinary calcium levels. After the low potassium diet, serum potassium fell in both groups, and serum phosphorus fell significantly in the BHT group.(ABSTRACT TRUNCATED AT 400 WORDS)
Increased platelet thromboxane A2/prostaglandin H2 receptors in patients with acute myocardial infarction.
Authors: Dorn G W , Liel N , Trask J L , Mais D E , Assey M E , Halushka P V
Published: June 2011

Platelets have been implicated in the formation of occlusive intracoronary thrombi leading to unstable angina pectoris and acute myocardial infarction. Evidence of platelet involvement in these syndromes includes increased thromboxane A2 synthesis during ischemic events and enhanced in vitro sensitivity to agonists. To determine the density and affinity of platelet thromboxane A2/prostaglandin H2 (TXA2/PGH2) receptors in patients with acute myocardial infarction and unstable angina pectoris, the maximum number of binding sites (Bmax) per platelet and the dissociation constant (Kd) of the TXA2/PGH2 receptor antagonist, [125I]-PTA-OH, was determined at equilibrium in washed platelets. Patients with acute myocardial infarction had a significantly (p = 0.006) higher Bmax (4,468 +/- 672 sites/platelet, n = 9) compared with controls (2,206 +/- 203 sites/platelet, n = 8). Restudied at a time when the patients' coronary artery disease was clinically stable, Bmax values for the myocardial infarction group had returned to within normal limits. The dissociation constant for [125I]-PTA-OH was not significantly different in the acute myocardial infarction patients compared with controls. In patients with acute myocardial infarction, the duration of chest pain was positively correlated (r = 0.71, p less than 0.02) with the number of [125I]-PTA-OH binding sites (Bmax). In vitro platelet sensitivity to the TXA2/PGH2 mimetic, U46619, was assessed in aggregation studies. The maximal velocity of aggregation (slope) correlated with platelet TXA2/PGH2 receptor number (r = 0.67, p less than 0.001) and was significantly higher (p less than 0.02) in the acute myocardial infarction patients compared with the other study groups. There was no significant difference in the aggregation EC50 values for the thromboxane mimetic U46619 between unstable angina, acute myocardial infarction, and control groups.(ABSTRACT TRUNCATED AT 250 WORDS)
Quantification and validation of left ventricular wall thickening by a three-dimensional volume element magnetic resonance imaging approach.
Authors: Beyar R , Shapiro E P , Graves W L , Rogers W J , Guier W H , Carey G A , Soulen R L , Zerhouni E A , Weisfeldt M L , Weiss J L
Published: June 2011

We have developed a method to quantify and map regional wall thickening throughout the left ventricle (LV) with magnetic resonance imaging. In contrast to methods that measure planar wall thickness and thickening, this method uses the three-dimensional (3D) geometry of the left ventricle to calculate the perpendicular thickness of the wall. We tested this method at three levels of increasing complexity using 1) phantom studies, 2) in vivo experiments in dogs with normal cardiac function, and 3) in vivo studies in dogs during acute ischemia. Experiments were conducted in 15 open-chest dogs imaged by a 0.38 T iron core magnet. Five short-axis images at end diastole and end systole were obtained with the spin echo technique by use of the QRS as a trigger for end diastole and the second heart sound, S2, to time end systole. After acquisition of preischemic images, acute ischemia was induced by either coronary artery ligation (n = 5) or intracoronary dental rubber injection (n = 5), which produced severe transmural ischemia. By use of computer-aided contouring of the endocardial and epicardial borders, each image was divided into 16 segments with radial lines originating from the midwall centroid. A 3D volume element was defined as that generated by connecting two matched planar segments in two adjacent image planes. This defined 64 volume elements comprising the entire left ventricle. Thickness and thickening before and during ischemia were then calculated by using the planar segments and the 3D volume elements. In phantom studies, the 3D method was accurate, independent of the angle of inclination of the image plane to the phantom wall, whereas the planar method showed considerable overestimation of thickness when the image plane was oblique to the phantom wall. In the dogs before induction of ischemia, the 3D method demonstrated the well-established normal taper in end-diastolic wall thickness from 1.10 +/- 0.02 cm at the base to 1.05 +/- 0.11 cm at the apex (p less than 0.01). By contrast, the planar method did not detect the decrease in thickness toward the apex (1.13 +/- 0.07 cm at the base vs. 1.16 +/- 0.14 cm at the apex, p = NS). During acute ischemia, thickening was calculated by both methods at the center of the ischemic zone defined by Monastral blue nonstaining and compared with the preischemic values.(ABSTRACT TRUNCATED AT 400 WORDS)
Two-dimensional echocardiographic determination of ventricular volumes in the fetal heart. Validation studies in fetal lambs.
Authors: Schmidt K G , Silverman N H , Van Hare G F , Hawkins J A , Cloez J L , Rudolph A M
Published: June 2011

The determination of ventricular volumes in the fetal heart from two-dimensional echocardiography (2DE) may give a better estimate of fetal ventricular size than simple diameter measurements, but the accuracy of this method has not been established. In fetal lambs, we tested whether ventricular volume calculations from 2DE using a biplane Simpson's rule algorithm are accurate. Calculations of left and right ventricular end-diastolic volumes from 2DE were compared with cast volumes of these ventricles. Also, at different levels of left atrial pressure, left ventricular stroke volumes calculated from 2DE were compared with stroke volumes measured simultaneously by an electromagnetic flowmeter. There was a good correlation between volumes determined from 2DE (y axis) and from casts (x axis) for both the left (r = 0.92; y = 0.2 + 1.1x; SEE = 0.19 ml) and right ventricle (r = 0.90; y = 0.7 + 0.9x; SEE = 0.21 ml). Left ventricular stroke volumes calculated from 2DE correlated well with those measured by the electromagnetic flowmeter (r = 0.87; y = 0.2 + 0.9x; SEE = 0.27 ml). Thus, calculation of fetal ventricular volumes from 2DE images using a biplane Simpson's rule method is feasible and accurate.
Antiarrhythmic actions of diltiazem during experimental atrioventricular reentrant tachycardias. Importance of use-dependent calcium channel-blocking properties.
Authors: Talajic M , Papadatos D , Villemaire C , Nayebpour M , Nattel S
Published: June 2011

The purpose of this study was to determine if the known frequency-dependent effects of diltiazem on inward calcium current result in selective actions during supraventricular tachycardia. These effects were evaluated by use of an experimental model of orthodromic atrioventricular reentrant tachycardia (AVRT). AVRT was induced in 15 dogs over a wide range of retrograde conduction times before and after two doses of diltiazem. Diltiazem produced a tachycardia-related suppression of atrioventricular nodal conduction resulting in greater efficacy for faster than for slower AVRTs. The degree of slowing for tachycardias that remained inducible after diltiazem administration was greater for AVRTs with a rapid initial rate (dose 1, 29%; dose 2, 40%) than for slower AVRTs (dose 1, 11%, p less than 0.01; dose 2, 18%, p less than 0.001). Rate-dependent AVRT slowing occurred because of a time-dependent phase of AH interval prolongation after the onset of tachycardia, which was observed only after diltiazem administration. to further clarify the mechanism of diltiazem's selective actions against faster tachycardias, its effects on the minimum pathway for reentry, or wavelength, were examined in four dogs. The ratio of refractory period to revolution time (RP/RT), an index of wavelength, was measured for each AVRT before and after diltiazem administration. Diltiazem increased the positive slope of the relation between RP/RT and the AVRT rate threefold compared with control (p less than 0.05). This rate-dependent effect prevented AVRT when RP/RT became greater than unity. In conclusion, rate-dependent atrioventricular node depression by diltiazem results in greater tachycardia slowing and higher rates of termination during atrioventricular reentrant tachycardias with faster initial rates and shorter retrograde conduction intervals.
Modification of sinus node function by epicardial laser irradiation in dogs.
Authors: Littmann L , Svenson R H , Gallagher J J , Bharati S , Lev M , Linder K D , Tatsis G P , Nichelson C
Published: June 2011

This study tested the feasibility of neodymium:YAG laser photocoagulation of selected sinus node areas to depress sinus rate responsiveness. In 14 open-chest dogs, origin of the sinus impulse (O point) was electrically mapped from the epicardium before and during isoproterenol infusion. Epicardial laser photocoagulation was applied to the O point observed during isoproterenol infusion and stepwise to remapped new O points until a 30 +/- 5% decrease in heart rate occurred. Long-term effects were assessed by Holter monitoring and electropharmacologic testing preoperatively and up to 10 weeks or 6 months. Mean (+/- SEM) percent decreases were observed at 10 weeks in the following parameters: average 24-hour heart rate, 17.4 +/- 5.0%; maximum heart rate on Holter, 30.5 +/- 3.5%; heart rate during pharmacologic autonomic blockade, 32.7 +/- 3.5%; and maximum heart rate on isoproterenol, 23.1 +/- 4.6% (all p less than 0.01). Curves with pacemaker recovery time plotted against control cycle length remained unchanged. Holter monitoring did not show excessive bradycardic episodes even after administration of propranolol. In three control dogs (sham operation), sinus node function remained unchanged. Histologic study of the irradiated area showed replacement by inflammatory cells, fibrosis, and cartilage formation with surrounding normal cells and occasional cells resembling pacemaker-like cells at the caudal end of the sinoatrial node. This study suggests that 1) map-guided graded laser photocoagulation of sinus node regions showing earliest activation during catecholamine stimulation successfully limits maximum heart rates without causing significant bradycardia, 2) the effects are long lasting, and 3) the remaining pacemaker behaves like the sinus node. Laser modification of sinus node function could become a form of nonpharmacologic heart rate control in patients with coronary artery disease undergoing surgery and in the syndrome of inappropriate sinus tachycardia.
Effects of resting vagal tone on accessory atrioventricular connections.
Authors: Morady F , Kadish A H , Schmaltz S , Rosenheck S , Summitt J
Published: June 2011

The purpose of this study was to determine the effects of resting vagal tone on accessory atrioventricular (AV) connections. Atropine (0.04 mg/kg) was administered to 13 patients with the Wolff-Parkinson-White syndrome and was found to have the following effects on the accessory AV connection: the anterograde block cycle length shortened from 305 +/- 51 to 279 +/- 54 msec (mean +/- SD; p less than 0.001); the retrograde block cycle length shortened from 288 +/- 57 to 251 +/- 50 msec (p less than 0.001); and the effective refractory period measured at a basic drive cycle length of 400 msec shortened from 295 +/- 45 to 265 +/- 47 msec in the anterograde direction (p less than 0.001) and from 283 +/- 18 to 261 +/- 12 msec in the retrograde direction (p less than 0.01). During atrial fibrillation, the mean ventricular cycle length decreased from 434 +/- 88 to 352 +/- 56 msec (p less than 0.001), and the shortest preexcited RR interval decreased from 302 +/- 56 to 256 +/- 43 msec (p less than 0.01). In another seven patients, propranolol (0.2 mg/kg) was administered before atropine, and atropine lengthened the anterograde block cycle length and the effective refractory period of the accessory AV connection; the magnitude of these effects was similar to that in the patients who did not receive propranolol. In conclusion, these data demonstrate that resting vagal tone exerts a direct depressant effect on accessory AV connections that does not require background sympathetic activity to be manifest.
Chest pain and coronary heart disease mortality among older men and women in three communities.
Authors: LaCroix A Z , Guralnik J M , Curb J D , Wallace R B , Ostfeld A M , Hennekens C H
Published: June 2011

Angina pectoris is a manifestation of coronary heart disease, yet little is known from clinical or epidemiologic studies about its prognosis in older populations. We investigated the relation of uncomplicated angina symptoms to risk of coronary heart disease mortality within 3 years in a prospective study of 8,359 people aged 65 and older residing in three communities. From baseline (1981-1983) to the third year of follow-up (1984-1986), there were 245 deaths from coronary heart disease. Three classifications of chest pain were defined using the Rose Questionnaire: nonexertional chest pain, chest pain on exertion (including angina), and angina. Exertional chest pain was a strong, independent predictor of coronary heart disease death for older men and women. There were no differences in the prognostic implications of this symptom between the sexes; the relative risks being 2.4 (95% confidence interval, 1.4-4.4) in men and 2.7 (1.7-4.2) in women. The risk of coronary heart disease mortality for those reporting chest pain on exertion was at least as high as that for participants whose symptoms met the Rose Questionnaire criteria for angina. The association between exertional chest pain and coronary heart disease mortality was independent of other coronary risk factors. The relation was specific for deaths from coronary heart disease, as there was no association between exertional chest pain and noncoronary causes of death. Chest pain on exertion conveys important prognostic information about risk of coronary death in older populations, regardless of gender.
Coronary vasomotor response to acetylcholine relates to risk factors for coronary artery disease.
Authors: Vita J A , Treasure C B , Nabel E G , McLenachan J M , Fish R D , Yeung A C , Vekshtein V I , Selwyn A P , Ganz P
Published: June 2011

In animals, acetylcholine dilates normal arteries and produces vasoconstriction in the presence of hypercholesterolemia, hypertension, or atherosclerosis, reflecting endothelial cell dysfunction. In patients with angiographically smooth coronary arteries, acetylcholine has been reported to produce both vasodilation and constriction. To test the hypothesis that the acetylcholine response relates to risk factors for coronary artery disease, acetylcholine 10(-8) to 10(-6) M was infused into the left anterior descending or circumflex coronary artery, and diameter changes were assessed with quantitative angiography in 34 patients with angiographically smooth coronary arteries. The acetylcholine response ranged from +37% (dilation) to -53% (constriction) at the peak acetylcholine dose. All coronary arteries dilated in response to nitroglycerin (26 +/- 17%), suggesting an abnormality of endothelial function in the patients with a constrictor response to acetylcholine. By multiple stepwise regression analysis, serum cholesterol (p less than 0.01), male gender (p less than 0.001), family history (p less than 0.05), age (p less than 0.05), cholesterol level (p less than 0.01), and total number of risk factors (p less than 0.0001) were independently associated with the acetylcholine response. Thus, coronary risk factors are associated with loss of endothelium-dependent vasodilation. The development of vasoconstriction is likely to be an abnormality of endothelial function that precedes atherosclerosis or an early marker of atherosclerosis not detectable by angiography.
Benefit of exercise conditioning for patients with peripheral arterial disease.
Authors: Hiatt W R , Regensteiner J G , Hargarten M E , Wolfel E E , Brass E P
Published: June 2011

Patients with atherosclerotic peripheral arterial disease (PAD) of the lower extremities have impaired walking ability due to exercise-induced muscle ischemia and the resultant pain of intermittent claudication. To evaluate the benefit of exercise training as a treatment for patients with PAD, as well as possible mechanisms associated with improvement, we randomly assigned 19 men with disabling claudication to treated and control groups. Treatment consisted of supervised treadmill walking (1 hr/day, 3 days/wk, for 12 weeks) with progressive increases in speed and grade as tolerated. Graded treadmill testing was performed to maximal toleration of claudication pain on entry and after 12 weeks of training to define changes in peak exercise performance. After 12 weeks, treated subjects had increased their peak walking time 123%, peak oxygen consumption 30%, and pain-free walking time 165% (all p less than 0.05). Control subjects had no change in peak oxygen consumption, but after 12 weeks, peak walking time increased 20% (p less than 0.05). In treated subjects, maximal calf blood flow (measured by a plethysmograph) increased 38 +/- 45% (p less than 0.05), but the change in flow was not correlated to the increase in peak walking time. Elevated plasma concentrations of acylcarnitines have been associated with the functional impairment of PAD and may reflect the metabolic state of ischemic skeletal muscle. In treated subjects, a 26% decrease in resting plasma short-chain acylcarnitine concentration was correlated with improvement in peak walking time (r = -0.78, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Complete recovery in plasma of enzymes lost from the heart after permanent coronary artery occlusion in the dog.
Authors: Hermens W T , van der Veen F H , Willems G M , Mullers-Boumans M L , Schrijvers-van Schendel A , Reneman R S
Published: June 2011

Plasma activities of creatine kinase (CK) and alpha-hydroxybutyrate dehydrogenase (HBD) were measured after permanent coronary artery occlusion in the dog. Cumulative release of enzymes in plasma was calculated from these data by using a previously validated two-compartment model for circulating enzymes. Regional myocardial ischemia was measured by injection of radiolabeled microspheres. After 48 hours, the dogs were killed, and a detailed map of left ventricular enzyme activity was obtained from 108 tissue samples. Cumulative release into plasma of CK and HBD was 96 +/- 20% and 112 +/- 26%, respectively, of the total activities depleted from the heart (mean +/- SD, n = 11). The scatter in these values is inherent to the calculations, and it is concluded that both enzymes are recovered completely in plasma and, thus, can be used as quantitative markers of injury. Discrepancies between this result and earlier reports on the recovery of CK are only partly apparent and can be explained partly by underestimation of the elimination rate of CK from plasma, irregardless of tissue edema and incomplete extraction of enzyme activity from tissue.
Class III antiarrhythmic agents have a lot of potential but a long way to go. Reduced effectiveness and dangers of reverse use dependence.
Authors: Hondeghem L M , Snyders D J
Published: June 2011

With regard to currently available class III agents, although their class III effect may reduce the likelihood of tachycardia initiation, their reverse use-dependent prolongation of action potential duration reduces their effectiveness during tachycardias and may even render them proarrhythmic, especially after long diastolic intervals. In contrast, agents that exhibit normal use-dependent prolongation of refractoriness hold great promise: While having relatively less effects on the normal heart beat, they could induce self-termination of a tachycardia. Prolongation of refractoriness can be achieved by lengthening of action potential duration and delaying recovery of excitability. Combination of these drug actions may yield important clinical applications.
Mechanism of cocaine-induced myocardial depression in dogs.
Authors: Fraker T D , Temesy-Armos P N , Brewster P S , Wilkerson R D
Published: June 2011

Cocaine causes pronounced depression of left ventricular function in conscious dogs immediately after intravenous administration. To examine this effect, 14 mongrel dogs were anesthetized with pentobarbital sodium (32 mg/kg) and instrumented with arterial and venous catheters and a Doppler blood flow transducer on the left circumflex coronary artery. Two weeks later, heart rate, blood pressure, coronary blood flow, and regional left ventricular ejection fraction (by two-dimensional echocardiography) were measured before and 1, 2, 5, and 10 minutes after cocaine (4 mg/kg i.v.), while the animals were fully conscious. Heart rate, blood pressure, and coronary blood flow were increased significantly at each time after cocaine. Regional ejection fraction, however, was depressed by 50 +/- 7%, 35 +/- 4%, and 21 +/- 4% at 1, 2, and 5 minutes after cocaine treatment, respectively. Ten minutes after cocaine treatment, regional ejection fraction had recovered to a level not significantly different from baseline. Because the observed myocardial depression after cocaine was accompanied by a large increase in the rate-pressure product, and presumably, myocardial oxygen consumption, this depression could have been secondary to increased myocardial oxygen demand not appropriately matched by an increase in coronary blood flow. To minimize the effects of cocaine on myocardial oxygen demand, a subset of six dogs received cocaine (4 mg/kg i.v.) while sedated with pentobarbital (25 mg/kg). In these dogs, cocaine did not significantly alter heart rate or blood pressure; however, regional ejection fraction was significantly depressed by 44 +/- 5% and 36 +/- 6% at 1 and 2 minutes after cocaine treatment, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Prostacyclin analogue iloprost decreases thrombolytic potential of tissue-type plasminogen activator in canine coronary thrombosis.
Authors: Nicolini F A , Mehta J L , Nichols W W , Saldeen T G , Grant M
Published: June 2011

Platelets play an important role in the formation of a coronary thrombus and reocclusion after thrombolysis. Therefore, we examined the thrombolytic potential of concomitant intravenous administration of potent platelet inhibitor iloprost, a prostacyclin analogue, with tissue-type plasminogen activator (t-PA; n = 8) and t-PA alone (n = 9) in dogs with an electrically induced occlusive coronary artery thrombus. t-PA (0.75 mg/kg) was given over 20 minutes, and iloprost (4 micrograms/kg) was given over 40 minutes. Reperfusion rate was 63% (five of eight dogs) in the t-PA plus iloprost group and 67% (six of nine dogs) in the t-PA alone group (p = NS). The time to thrombolysis (or reperfusion) in the t-PA plus iloprost group was almost twice as great as in the t-PA alone group (33.0 +/- 13.3 vs. 18.5 +/- 6.7 minutes, mean +/- SD, p less than 0.02), and the duration of reperfusion was much shorter (3.4 +/- 1.8 vs. 39.3 +/- 17.4 minutes, p less than 0.005). Peak coronary artery blood flow after reperfusion in the t-PA plus iloprost group was also less (20 +/- 17 ml/min) than in the t-PA alone group (58 +/- 21 ml/min, p less than 0.005). Reocclusion occurred in all dogs given t-PA with iloprost despite potent synergistic platelet inhibitory effects of t-PA and iloprost, whereas four of six dogs given t-PA alone reoccluded. Neither regimen exerted a significant beneficial effect on regional myocardial shortening during coronary reperfusion. Plasma levels of t-PA were lower when iloprost was given with t-PA (1,022 +/- 360 vs. 1,459 +/- 270 ng/ml in t-PA alone group, p less than 0.05). The detrimental effects of iloprost identified in this study may relate to the reduction in plasma t-PA concentrations by its degradation in the liver caused by the prostacyclin analogue iloprost.
Silent ischemia during daily life is an independent predictor of mortality in stable angina.
Authors: Deedwania P C , Carbajal E V
Published: June 2011

We prospectively examined the prognostic significance of silent myocardial ischemia detected by ambulatory electrocardiogram (ECG) monitoring during daily life in 107 patients with long-term stable angina who were symptomatically controlled on conventional antianginal agents. Forty-six patients (group 1) demonstrated one or more episodes (87% silent) of myocardial ischemia; the remaining 61 patients (group 2) had no ischemic ST segment changes. During the mean follow-up period of 23 +/- 8 months, 11 cardiac deaths (five sudden and six nonsudden) occurred in group 1, and five cardiac deaths (all nonsudden) occurred in group 2. Kaplan-Meier survival analysis between the groups confirmed that patients with silent ischemia (group 1) had worse prognoses during the follow-up period (p = 0.023). Although the higher incidence of hypertension, smoking, hypercholesterolemia, and diabetes in our patients might reflect a more sickly population of stable angina patients, the multivariate Cox's hazard function analysis of these and other variables including Q waves on ECG, exercise parameters, and ambulatory ECG findings revealed presence of silent ischemia during daily life as the most powerful and independent predictor of cardiac mortality (p = 0.01). These data indicate that, in such patients with stable angina, silent myocardial ischemia occurs frequently during treatment with conventional antianginal drugs and identifies a subset of patients who are at high risk of cardiac death.
Prognostic significance of the electrocardiogram after Q wave myocardial infarction. The Framingham Study.
Authors: Wong N D , Levy D , Kannel W B
Published: June 2011

The prognostic value of abnormalities on the electrocardiogram (ECG) present 1 year after initial myocardial infarction (MI) is examined in relation to reinfarction and coronary death throughout 32 years (mean, 10.1 years) of follow-up in the Framingham Heart Study. Resting 12-lead ECGs were available in 251 survivors (190 men and 61 women) of clinically recognized Q wave MI. The ECG reverted to normal in 31 (12.4%) cases and was abnormal but without Q waves in 37 (14.7%). Q waves persisted without other significant abnormalities in 108 (43.0%) and with other abnormalities in 75 (29.9%) cases. Electrocardiographic abnormalities at follow-up were more common in women and in those persons whose initial MI was anterior as compared with inferior. Nonspecific T wave, ST segment changes, and electrocardiographic left ventricular hypertrophy on the ECG before or after MI were powerful predictors (p less than 0.01) of coronary death. The relation of these residual post-MI electrocardiographic findings to reinfarction and coronary death was assessed by Cox regression analysis. The follow-up electrocardiographic status was unrelated to the risk of subsequent reinfarction. Subjects who lost Q wave evidence of MI but whose ECG continued to show evidence of repolarization abnormalities, left ventricular hypertrophy, or blocked intraventricular conduction were at a 3.5-fold increased risk (p less than 0.01) of coronary death as compared with those reverting to a normal ECG. Persons with a persistent Q wave MI accompanied by these abnormalities were at a 2.7-fold excess risk (p = 0.01) of coronary death as compared with those with a normalized ECG. These findings remained significant when considering age and standard coronary risk factors. The presence of other electrocardiographic abnormalities without persistent Q waves yields a worse prognosis than a Q wave persisting alone. The prognostic value of a follow-up ECG with abnormalities other than a persistent Q wave MI also remained after considering the effects of left ventricular hypertrophy and cardiac enlargement on x-ray, functional classification, and diuretic usage. Specific electrocardiographic abnormalities present before infarction, however, were potent indicators of long-term prognosis prognosis and diminished the importance of the follow-up ECG. Although survival after initial MI is improved only if the ECG reverts to normal, information on electrocardiographic abnormalities before MI can be especially useful in evaluating long-term risk.
Early alterations of the baroreceptor control of heart rate in patients with acute myocardial infarction.
Authors: Osculati G , Grassi G , Giannattasio C , Seravalle G , Valagussa F , Zanchetti A , Mancia G
Published: June 2011

Experimental coronary occlusion is accompanied by an acute impairment of the baroreceptor-heart rate reflex. This study was planned to determine whether this impairment also occurs in humans. In 30 patients admitted to a coronary care unit for an anterior (n = 14) or inferior (n = 16) transmural myocardial infarction (MI), we measured 1) the increase in RR interval induced by stimulating carotid baroreceptors through progressive reductions in neck chamber pressure, 2) the increase in RR interval induced by stimulating arterial baroreceptors through intravenous boluses of phenylephrine, and 3) the reduction in RR interval induced by deactivating arterial baroreceptors through intravenous boluses of nitroglycerin. Measurements were performed 49.5 +/- 2.4 hours (mean +/- SEM) after the MI. The results were compared with those of five age-matched patients admitted to the coronary care unit for chest pain and found free from ischemic heart disease. The sensitivity of the carotid baroreceptor-heart rate reflex (slope of the linear regression of RR interval over neck pressure changes) was markedly less in MI than in control patients (3.8 +/- 0.5 vs. 5.9 +/- 0.6 msec/mm Hg, p less than 0.05), the reduction being similar in patients with anterior and inferior MI. This was the case also for the baroreflex sensitivity measured by the phenylephrine and the nitroglycerin methods (slope of the linear regression of RR interval over systolic blood pressure changes). However, 10.2 +/- 0.3 days later, the baroreflex sensitivity measured by all three methods increased significantly (p less than 0.05 or 0.01) and became similar to that of control subjects, which showed no significant change from the early to the late period after admission into the coronary care unit. Thus, MI is accompanied by an acute marked impairment of the baroreceptor control of the heart in humans, and this is the case both for an anterior and an inferior MI. The impairment is largely transient in nature, however, and a clear-cut recovery of the baroreflex can be seen a few days later.
Fibrosis in the transplanted heart and its relation to donor ischemic time. Assessment with polarized light microscopy and digital image analysis.
Authors: Pickering J G , Boughner D R
Published: June 2011

Long-distance procurement of cardiac allografts is commonly used to increase the supply of donor organs but has recently been associated with the development of impaired diastolic function. Therefore, the effect of the total ischemic duration on myocardial fibrosis was quantitatively evaluated in 36 cardiac transplant recipients in whom the ischemic time ranged from 70 to 363 (mean, 189 +/- 83) minutes. Interstitial collagen was quantified with polarization microscopy and digital image analysis in 115 endomyocardial biopsy specimens taken 5-10 days after surgery. The technique, developed for this study, showed excellent correlation with hydroxyproline analysis (r = 0.98, p less than 0.001). Collagen volume fraction in biopsy specimens from the transplanted hearts was significantly greater than that in biopsy samples from seven normal, age-matched autopsy hearts (4.7 +/- 1.9% vs. 2.9 +/- 0.6%, p less than 0.02). The degree of fibrosis correlated with the total ischemic time (r = 0.60, p less than 0.001). Donor age ranged from 10 to 51 years and did not correlate with the degree of fibrosis. No relation was found between the corresponding collagen content and right atrial pressure, pulmonary artery wedge pressure, or cardiac output measured at the time of biopsy. Myocyte damage was observed in eight of the 36 patients and was characterized by a striking loss of muscle birefringence. We conclude that cardiac allograft fibrosis may be identified shortly after transplantation and is dependent on the total ischemic duration.
Detrimental sequelae on the hemodynamics of the upper left limb after subclavian flap angioplasty in infancy.
Authors: van Son J A , van Asten W N , van Lier H J , Daniëls O , Vincent J G , Skotnicki S H , Lacquet L K
Published: June 2011

The long-term effect of two surgical techniques for repair of coarctation of the aorta in infancy, namely, resection and end-to-end anastomosis (RETE) and subclavian flap angioplasty (SFA) on the blood supply of the upper left limb, was quantified by Doppler spectrum analysis of blood flow velocities in the left brachial artery at rest and during postocclusive reactive hyperemia. Twenty-three patients participated in this study: nine patients after SFA (median age, 8 years), 14 patients after RETE (median age, 8 years), and 10 control subjects (median age, 9.5 years). At rest, a highly significant decrease of blood flow velocities in the left brachial artery was measured in all patients of the SFA group compared with those of the RETE and control groups, as documented by various Doppler spectrum parameters: maximal frequency of advancing curve (p = 0.0001), pulsatility index (p = 0.0005), and resistance index (p = 0.039). During reactive hyperemia, a moderate capacity of physiologic augmentation of blood flow velocities was observed in five patients of the SFA group. This capacity was marginal in two patients with complaints of claudication in the left upper limb during strenuous exercise, which can be related to the number of branches of the left subclavian artery ligated during operation. This study indicates that SFA in infancy may lead to compromised hemodynamics of the upper left limb with potential for symptoms of ischemia during exercise.
Determinants of survival and left ventricular performance after mitral valve replacement. Department of Veterans Affairs Cooperative Study on Valvular Heart Disease.
Authors: Crawford M H , Souchek J , Oprian C A , Miller D C , Rahimtoola S , Giacomini J C , Sethi G , Hammermeister K E
Published: June 2011

To determine how survival and clinical status were related to left ventricular (LV) size and systolic function after mitral valve replacement, 104 patients (48 mitral regurgitation [MR], 33 mitral stenosis [MS], and 23 MS/MR) with isolated mitral valve replacement were evaluated before and after surgery. Preoperative hemodynamic abnormalities by cardiac catheterization were improved 6 months after surgery in all three patient groups. The patients with MR exhibited reductions in LV end-diastolic volume index (EDVI) (117 +/- 51 to 89 +/- 27 ml/m2, p less than 0.001) and ejection fraction (EF) (0.56 +/- 0.15 to 0.45 +/- 0.13, p less than 0.001); however, the ratio of forward stroke volume to end-diastolic volume increased (0.32 +/- 0.21 to 0.45 +/- 0.17, p less than 0.001) because of the elimination of regurgitant volume. Survival analysis revealed that mortality was significantly higher in MS or MS/MR patients with postoperative EDVI more than 101 ml/m2 (p less than 0.001 and p less than 0.042, respectively) and in MR patients with postoperative EF less than or equal to 0.50 (p less than 0.031). Also, the majority of patients with MR or MS/MR and postoperative EDVI more than 101 ml/m2 and EF less than or equal to 0.50 were in New York Heart Association class III or IV. Multivariate logistic regression analysis in the patients with MR revealed that the strongest predictor of postoperative EF was preoperative EF (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
Left-to-right atrial shunting after percutaneous mitral valvuloplasty. Incidence and long-term hemodynamic follow-up.
Authors: Cequier A , Bonan R , Serra A , Dyrda I , Crépeau J , Dethy M , Waters D
Published: June 2011

To assess the incidence and long-term evolution of left-to-right atrial shunting (AS) after the performance of percutaneous mitral valvuloplasty (PMV), venovenous indicator dilution curves and right heart oximetric measurements were obtained in 68 consecutive patients before and after successful PMV. The procedure increased the mitral valve area (p less than 0.0001) and decreased the mitral gradient (p less than 0.0001). No AS was detected before PMV, but it was detected immediately after PMV. Oximetry identified AS in 17 patients (25%), and dilution curves identified AS in an additional 25 (total, 62%). The ratio of mean pulmonary to systemic blood flow (Qp/Qs) was 1.31 +/- 0.2, and in six patients (9%), the ratio was 1.5 or greater. Among nine clinical, 20 hemodynamic, and six procedural variables, stepwise logistic regression analysis selected the following as independent predictors of AS: smaller increases in valve area (p = 0.01) after PMV, absence of previous surgical commissurotomy (p = 0.02), mitral valve calcification (p = 0.02), and smaller left atria (p = 0.06). Among the 33 patients recatheterized at 6 months, oximetry had detected AS in 10, and dilution curves detected AS in an additional nine (total, 58%) immediately after PMV. At 6 months, AS had decreased or disappeared in 14 of these patients (74%), had increased in three (16%), and was unchanged in two (10%). Overall, at 6 months, oximetry identified AS in three patients, and dilution curves identified AS in an additional 13 (total, 48%). AS was detected at 6 months in only three patients but was not detected immediately after PMV. Although AS is very frequent immediately after PMV, Qp/Qs is usually less than 1.5. The appearance of shunting correlates with patient characteristics and with less improvement in valve area after PMV. Atrial shunting usually persists at 6 months, but its severity almost always decreases.
The safety of intravenous dipyridamole thallium myocardial perfusion imaging. Intravenous Dipyridamole Thallium Imaging Study Group.
Authors: Ranhosky A , Kempthorne-Rawson J
Published: June 2011

Clinical data on 3,911 patients were collected from 64 individual investigators to evaluate the safety of intravenous dipyridamole-thallium imaging as an alternative to exercise thallium imaging for the evaluation of coronary artery disease. There were two deaths because of myocardial infarctions, two nonfatal myocardial infarctions, and six cases of acute bronchospasm. Chest pain occurred in 770 patients (19.7%). Headache and dizziness were reported by 476 patients (12.2%) and 460 patients (11.8%), respectively. ST-T changes on the electrocardiogram were seen in 292 patients (7.5%). Use of parenteral aminophylline to treat adverse events associated with intravenous dipyridamole brought complete relief of symptoms in 439 of 454 patients (96.7%). There is a potential for increased risk for serious ischemic events in patients with a history of unstable angina who are administered intravenous dipyridamole. In patients with acutely unstable angina (i.e., continuing chest pain) or in the acute phase of myocardial infarction, use of intravenous dipyridamole in thallium scintigraphy should be avoided. There is also an increased risk for bronchospasm in patients with a history of asthma; acute bronchospasm can be relieved immediately by administration of aminophylline. These results demonstrate that intravenous dipyridamole-thallium scintigraphy is a relatively safe, noninvasive technique for the evaluation of coronary artery disease.
Exercise performance after repair of anomalous origin of the left coronary artery from the pulmonary artery.
Authors: Paridon S M , Farooki Z Q , Kuhns L R , Arciniegas E , Pinsky W W
Published: June 2011

Eleven patients underwent exercise testing after operative repair of anomalous origin of the left coronary artery from the pulmonary artery. Five patients repaired after 2 years of age comprised a childhood surgery group, and six patients repaired before 2 years of age comprised an infant surgery group. All patients were exercised using either a treadmill or electronically braked bicycle with simultaneous thallium 201 scintigraphy. Oxygen consumption, carbon dioxide production, pulmonary functions, and electrocardiogram were all monitored continuously. Pulmonary reserve was normal in all patients. Based on heart rate reserve, respiratory exchange ratio, and oxygen-consumption response to work load, two patients in the infant surgery group stopped exercise before achieving maximum aerobic capacity. All remaining patients achieved their maximum aerobic capacity. There was no difference in work rate or oxygen consumption during exercise between the infant and childhood surgical group. Four patients (two in each surgical group) had an impaired chronotropic response to exercise. Three of these four patients demonstrated perfusion defects by thallium scintigraphy. Thallium scintigraphy was normal in all remaining patients. Electrocardiographic abnormalities were noted in seven of 11 patients having ventricular arrhythmias or ST segment depression. It is concluded from this study that exercise performance after repair of anomalous origin of the left coronary artery from the pulmonary artery is not affected by the age at which surgery is performed. Exercise is frequently associated with electrocardiographic evidence of abnormal myocardial perfusion despite frequently negative simultaneous 201Tl scintigraphy.
Changes in lipoprotein subfractions during diet-induced and exercise-induced weight loss in moderately overweight men.
Authors: Williams P T , Krauss R M , Vranizan K M , Wood P D
Published: June 2011

We studied separately the effects of weight loss by calorie restriction (dieting) and by calorie expenditure (primarily, running) on lipoprotein subfraction concentrations in sedentary, moderately overweight men assigned at random into three groups as follows: exercise without calorie restriction (n = 46), calorie restriction without exercise (n = 42), and control (n = 42). Plasma lipoprotein mass concentrations were measured by analytic ultracentrifugation for flotation rates (F0(1.20), S0f) within high density lipoprotein (HDL) (F0(1.20) 0-9), low density lipoprotein (LDL) (S0f 0-12), intermediate density lipoprotein (IDL) (S0f 12-20), and very low density lipoprotein (VLDL) (S0f 20-400) particle distributions. Particle diameter and flotation rate of the most abundant LDL species were determined by nondenaturing polyacrylamide gradient gel electrophoresis and analytic ultracentrifugation, respectively. During the 1-year trial, the exercisers ran (mean +/- SD) 15.6 +/- 9.1 km/wk, and the dieters ate 340 +/- 71 fewer kilocalories per day than at baseline. Total body weight was reduced significantly more in dieters (-7.2 +/- 4.1 kg) and exercisers (-4.0 +/- 3.9 kg) than controls (0.6 +/- 3.7 kg). As compared with mean changes in controls, the exercisers and dieters significantly increased HDL2 mass (48.6% and 47.1%, respectively), decreased VLDL mass (-23.9% and -25.5%), and increased LDL peak particle diameter (2.4 and 3.2 A). When adjusted to an equivalent change in body mass index by analysis of covariance, 1) exercise-induced and diet-induced weight loss produced comparable mean changes in the mass of small LDL and VLDL, and in LDL peak particle diameter; 2) the exercisers versus control group difference in HDL2 was attributed to the exercisers' reduced body mass index; and 3) HDL2 increased significantly less in dieters than in exercisers. In dieters, low calorie intake might mitigate the effects of weight loss on HDL2.
Autonomic function in hypertension. Are there racial differences?
Authors: Parmer R J , Cervenka J H , Stone R A , O'Connor D T
Published: June 2011

Previous biochemical assessment of sympathetic nervous system activity including plasma catecholamines, plasma renin activity, and plasma dopamine-beta-hydroxylase levels has suggested racial differences in the contribution of the sympathetic nervous system to the pathogenesis or maintenance of hypertension. We, therefore, performed physiological and pharmacological studies in white and black subjects with essential hypertension and their age-matched normotensive counterparts to assess autonomic and sympathetic nervous system function. One hundred one male subjects (47 white hypertensive, 17 black hypertensive, 22 white normotensive, and 15 black normotensive subjects) were evaluated for baroreceptor reflex sensitivity to low-pressure (amyl nitrite inhalation) and high-pressure (phenylephrine infusion) stimuli; cold pressor test heart rate and blood pressure responses; and blood pressure response to phentolamine alpha-adrenergic blockade. Hypertensive subjects exhibited an increase in resting heart rate, a decrease in baroreceptor reflex sensitivity, and an exaggerated decline in mean arterial pressure in response to phentolamine. These abnormalities were present to a comparable degree in black and white hypertensive subjects. Cold pressor testing revealed greater increases in heart rate in blacks as compared with whites; however, this racial difference was present regardless of blood pressure status, occurring in black normotensive and black hypertensive subjects to a comparable degree. Cold pressor test blood pressure increments were similar in the four groups. We conclude that both white hypertensive and black hypertensive subjects demonstrate similar abnormalities in autonomic and sympathetic nervous system function including blunting of baroreceptor reflex sensitivity and an increased alpha-adrenergic receptor participation in blood pressure maintenance. The results do not suggest major racial differences in autonomic pathogenetic mechanisms in hypertension.