bluuebunny/crossref_metadata_2025 huggingface dataset:
The role of intracoronary thrombus in unstable angina: angiographic assessment and thrombolytic therapy during ongoing anginal attacks.
Authors: Gotoh K , Minamino T , Katoh O , Hamano Y , Fukui S , Hori M , Kusuoka H , Mishima M , Inoue M , Kamada T
Published: June 2011

Intracoronary thrombus is regarded as a potentially important factor in the etiology of unstable angina, but the incidence of intracoronary thrombus in unstable angina has not been clearly defined. To determine the occurrence of intracoronary thrombus during ongoing angina pectoris, coronary angiography was performed during spontaneous ischemic attacks in 37 patients with prolonged rest angina. All patients exhibited significant (greater than 50%) stenoses of at least one major coronary artery. Of the 37 patients, 21 (57%) had intracoronary thrombus in major coronary arteries, whereas 14 (38%) had fixed narrowings without evidence of intracoronary thrombus and two exhibited coronary spasm. ST segment elevation was observed in 16 of 21 patients with thrombus and in all of the patients with coronary spasm, but all the patients with organic stable obstruction showed ST segment depression. Twenty of the 21 patients with thrombus improved after thrombolytic therapy with intracoronary injection of urokinase; obstructed arteries were reopened, or narrowings were attenuated, with relief of ischemic symptoms. In patients with fixed obstructions, the rate-pressure product during active symptoms was significantly higher than during an asymptomatic period, indicating that a transient increase in myocardial oxygen demand may contribute to the ischemic attack in these patients. A high incidence (71%) of recurrent symptoms was observed in patients with intracoronary thrombus even after successful thrombolysis, in contrast to a much lower incidence (36%) in those without intracoronary thrombus. Myocardial infarction within 4 weeks after catheterization was observed more frequently in patients with intracoronary thrombus (24%) than in those without thrombus (7%).(ABSTRACT TRUNCATED AT 250 WORDS)
The relationship between left ventricular systolic function and congestive heart failure diagnosed by clinical criteria.
Authors: Marantz P R , Tobin J N , Wassertheil-Smoller S , Steingart R M , Wexler J P , Budner N , Lense L , Wachspress J
Published: June 2011

There is no uniformly accepted clinical definition for congestive heart failure (CHF), although criteria have been published by various groups. There is also no reference standard for CHF, although left ventricular ejection fraction (LVEF) gives a quantitative assessment of systolic function and is useful in predicting prognosis. To determine the relationship between LVEF and clinically diagnosed CHF, we compared resting LVEF determined by radionuclide ventriculography with diagnosis of CHF by clinical criteria in 407 patients, based on clinical data collected by a cardiology fellow. Of 153 patients with a low LVEF (less than or equal to 0.40), 30 (20%) met none of the criteria for CHF. Conversely, of 204 patients with normal LVEF (greater than or equal to 0.50), 105 (51%) met at least one of the criteria. We conclude that different criteria for CHF will have varying utility depending on the population being examined, and that a combination of clinical features and an objective measure of cardiac performance is needed to diagnose CHF.
Relationship between the 12-lead electrocardiogram during ventricular tachycardia and endocardial site of origin in patients with coronary artery disease.
Authors: Miller J M , Marchlinski F E , Buxton A E , Josephson M E
Published: June 2011

Previous studies in patients with sustained ventricular tachycardia (VT) have demonstrated the efficacy of surgical and catheter-mediated ablative procedures based on activation mapping during VT. Since extensive preoperative or intraoperative mapping may be impractical due to time constraints or patient intolerance, we sought to define characteristics of the 12-lead electrocardiogram (ECG) during VT that could suggest a particular endocardial region of origin and thus facilitate mapping studies. Endocardial mapping was performed during 182 VTs in 108 patients with prior myocardial infarction of either the anterior or inferior wall. Endocardial sites of origin (sites from which greater than or equal to 40 msec of presystolic electrical activity was consistently recorded) were identified with use of catheter (154 VTs) or intraoperative (85 VTs) activation mapping (both methods used in 57 Vts). Twelve-lead ECGs obtained during these VTs were characterized by four features: location of infarction, bundle branch block type configuration, quadrant of QRS axis, and precordial R wave progression pattern. A specific combination of these four features was associated with a particular endocardial region containing the mapped site of origin in 87 VTs (48% of total). An association (greater than or equal to 70% positive predictive accuracy) was more likely to be found in the presence of left, as opposed to right, bundle branch block type patterns (53/73 [73%] vs 34/109 [31%]; p less than .001) and in the presence of VT related to inferior, as opposed to anterior, infarction (40/54 [74%] vs 47/128 [37%]; p less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)
ST segment elevation with exercise: a marker for poor ventricular function and poor prognosis. Coronary Artery Surgery Study (CASS) confirmation of Seattle Heart Watch results.
Authors: Bruce R A , Fisher L D , Pettinger M , Weiner D A , Chaitman B R
Published: June 2011

The functional and prognostic significance of exercise-induced ST elevation (by computer averaging) in ambulatory patients with coronary heart disease was recently reported for 181 patients in the Seattle Heart Watch (SHW). To further evaluate this, 3050 approximately similar patients enrolled in CASS were analyzed with respect to initial findings, survival, and incidence of secondary coronary events over the next 6 years. The ST elevation responses in CASS patients were classified by visual interpretation of 1 mm or more, whereas the SHW patients were identified by voltage greater than 0 mV. Accordingly, prevalence of exercise-induced ST elevation was lower in CASS patients, but they had greater frequencies of prior myocardial infarction and left ventricular enlargement and dysfunction. The poor survival was similar in the subgroup with ST elevation during exercise and recovery in CASS and SHW. Although not an independent predictor when invasive variables are known, ST elevation emerges as a useful predictor when exercise testing is performed before diagnostic invasive studies.
Energy, current, and success in defibrillation and cardioversion: clinical studies using an automated impedance-based method of energy adjustment.
Authors: Kerber R E , Martins J B , Kienzle M G , Constantin L , Olshansky B , Hopson R , Charbonnier F
Published: June 2011

The purposes of this study were two. First, we wanted to evaluate in patients a technique for automated adjustment of selected energy for defibrillation or cardioversion based on transthoracic impedance. Second, we wanted to define the relationship of peak current and shock success in various arrhythmias. Applying a previously validated method of predicting transthoracic impedance in advance of any shock, we modified defibrillators to automatically double the operator-selected energy if the predicted impedance exceeded 70 omega. Success rates of shocks given for ventricular and atrial arrhythmias from these modified energy-adjusting defibrillators were compared with success rates for shocks given from standard defibrillators. We prospectively collected data on 347 patients who received a total of 1009 shocks. Low-energy (100 J) shocks given to high-impedance (greater than or equal to 70 omega) patients had a poor success rate; in such high-impedance patients significant improvement in shock success rate was achieved by the energy-adjusting defibrillators. For example, when 100 J shocks were selected for high-impedance patients in ventricular fibrillation the energy-adjusting defibrillators achieved a shock success rate of 75%, whereas standard defibrillators achieved a shock success rate of only 36% (p less than .01). Similar improvements were seen for ventricular tachycardia and atrial fibrillation. Thus, automated energy adjustment based on transthoracic impedance is a beneficial approach to defibrillation and cardioversion. For ventricular fibrillation, atrial fibrillation, and atrial flutter there was a clear relationship between peak current and shock success.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiopulmonary adaptation at rest and during exercise 10 years after Mustard atrial repair for transposition of the great arteries.
Authors: Musewe N N , Reisman J , Benson L N , Wilkes D , Levison H , Freedom R M , Trusler G A , Canny G J
Published: June 2011

Discordance exists between apparently reduced systemic right ventricular function and the reported asymptomatic state of many patients after atrial repair for transposition of the great arteries. To evaluate this clinical observation, cardiopulmonary response to exercise in 17 asymptomatic patients with no significant postoperative hemodynamic abnormalities was assessed by upright bicycle ergometry according to a modified Jomes protocol 11.5 +/- 1.5 years after Mustard atrial repair. Seventeen age- and sex-matched normal adolescents constituted the control group. Incremental exercise was performed to determine maximum work capacity, heart rate, blood pressure, oxygen saturation, and minute ventilation. Cardiac output was computed at rest and during steady-state exercise by a carbon dioxide rebreathing method at 50% of the maximum workload achieved during incremental exercise. Height and weight were similar in patients and controls (p greater than .05). Resting pulmonary function variables were normal in all subjects. At peak exercise, respiratory quotient was greater than 1 in both patients and controls (1.12 +/- 0.09 and 1.09 +/- 0.08 respectively, p greater than .05). Patients achieved a lower peak heart rate (172 +/- 14 vs 185 +/- 11 beats/min, p less than .01), lower maximum work capacity (2.3 +/- 0.6 vs 3.3 +/- 0.7 W/kg, p less than .01). The ratio of minute ventilation at peak exercise to maximum resting voluntary ventilation was normal (less than or equal to 80%) in both groups. The ventilatory equivalent for oxygen was similar at rest, but significantly higher in patients than in control subjects at peak exercise (42 +/- 7 vs 36 +/- 5, p less than .006).(ABSTRACT TRUNCATED AT 250 WORDS)
Reduction of atrial natriuretic factor circulating levels by endogenous sympathetic activation in hypertensive patients.
Authors: Volpe M , DeLuca N , Atlas S A , Camargo M J , Indolfi C , Lembo G , Trimarco B , Condorelli M , Laragh J H
Published: June 2011

The effects of endogenous activation of sympathetic nervous system on systemic and regional hemodynamics and on plasma levels of atrial natriuretic factor (ANF) were studied in subjects with essential hypertension. Stimulation of sympathetic nervous system was reflex-induced by a selective deactivation of carotid baroreceptors obtained by increasing external neck-tissue pressure (NTP) by means of a neck chamber. The effects of graded levels (+30, +45, and +60 mm Hg) and one single and sustained level (+45 mm Hg for 15 min) of NTP were studied. As expected, NTP caused reflex increases in blood pressure, heart rate, and forearm vascular resistance, whereas atrial pressures did not change significantly and cardiac output tended to increase. In the studies based on graded levels of NTP, immunoreactive ANF (irANF) progressively fell (from 31.7 +/- 10 to 13.3 +/- 4 fmol/ml; p less than .05) and the changes in irANF were significantly correlated with those observed in FVR (r = -.671, p less than .001). Both hemodynamic and irANF changes were prevented by adrenergic blockade (phentolamine + propranolol). During +45 mm Hg NTP for 15 min, the levels of irANF fell both in the pulmonary artery and in the inferior vena cava. The irANF arteriovenous difference also fell during this maneuver. These data show that, in hypertensive patients, factors other than atrial wall tension may influence ANF release. They also show that endogenous sympathetic activation may reduce ANF release.
Demonstration of a widely distributed atrial pacemaker complex in the human heart.
Authors: Boineau J P , Canavan T E , Schuessler R B , Cain M E , Corr P B , Cox J L
Published: June 2011

Atrial depolarization was analyzed in 14 patients with the Wolff-Parkinson-White syndrome undergoing surgery to ablate accessory atrioventricular pathways associated with tachyarrhythmias. Bipolar potentials were recorded simultaneously from 156 atrial epicardial electrodes arranged in three templates to fit the anterior and posterior aspects of both atria. Spontaneous or sinus rhythms were recorded, as were atrial escape rhythms after overdrive pacing at rates of 150 and 200 beats/min. Atrial activation maps revealed different patterns of impulse initiation varying from typical unifocal sinus node impulse origin, unifocal extranodal impulse origin, and multicentric impulse origin from two to four widely distributed atrial pacemaker sites. In subjects demonstrating only unifocal impulse origin during control or sinus rhythm, other widely divergent pacemaker sites were recorded in other maps during subsequent rhythms. In addition to sites located at the upper superior vena cava-right atrium junction, pacemakers also dominated at sites anterior and inferior to the sinus node region during both control and escape depolarizations. Most of the subjects were found to have two or more pacemaker sites when maps of all control and postpacing conditions were analyzed. The right atrial pacemaker region encompassed a zone of 7.5 X 1.5 cm centered about the long axis of the sulcus terminalis posteriorly and the precaval band anteriorly. An unexpected finding was the participation of left atrial escape pacemakers. The functional behavior of both the control and escape pacemakers, as assessed by sinus node recovery time, was normal, indicating physiologic operation of the extranodal sites as part of an overall system of distributed pacemakers involved in the control of rate. Although functional assessment was limited in these initial patient studies, correspondence with similar observations in extensive previous canine studies supports the concept of a widely distributed atrial pacemaker complex in man.
Diagnostic value of the ratio of recovery systolic blood pressure to peak exercise systolic blood pressure for the detection of coronary artery disease.
Authors: Acanfora D , De Caprio L , Cuomo S , Papa M , Ferrara N , Leosco D , Abete P , Rengo F
Published: June 2011

It has been previously reported that at treadmill exercise testing an abnormal ratio of recovery systolic blood pressure (SBP) to peak exercise SBP is more sensitive than exercise-induced angina or ST segment depression for diagnosing coronary artery disease (CAD). To investigate whether the SBP ratio keeps its diagnostic value during upright bicycle exercise, we evaluated the ratio of postexercise SBP to peak SBP in 73 patients with angiographically documented CAD and in 48 patients with normal coronary arteries (OV group) undergoing maximal stress testing on a bicycle ergometer. Three minutes after exercise ended, SBP ratio was significantly higher in the CAD than in the OV group (0.79 +/- 0.1 vs 0.71 +/- 0.08; p less than .001). Setting the upper normal limits of the recovery SBP ratio at 2 SDs from the mean for the OV group (SBP ratio = 0.98 and 0.88 at 1 and 3 min after exercise, respectively), with an increase or no change in SBP ratio at between 1 and 3 min of recovery considered an abnormal response, the sensitivity of SBP ratio was 30%, the specificity was 83%, and the accuracy was 51%. The respective values for ST depression were 81% (p less than .0001 vs SBP ratio), 48% (p less than .001 vs SBP ratio), and 67% (p less than .01 vs SBP ratio). Thus, for bicycle ergometer exercise testing, ST segment depression seems to be more accurate than SBP ratio in diagnosing CAD.
Delayed afterdepolarizations elicited in vivo by left stellate ganglion stimulation.
Authors: Priori S G , Mantica M , Schwartz P J
Published: June 2011

Activation of cardiac sympathetic nerves is recognized as a triggering factor for cardiac arrhythmias. However, the mechanisms involved have only been speculated. Because evidence from studies in vitro has established a relation between catecholamines, delayed afterdepolarizations (DAD), and triggered rhythms, it seemed possible that in vivo adrenergic activation also might lead to the development of DAD. Because very little evidence was available for DAD in vivo, we have evaluated whether monophasic action potential (MAP) recording with a contact electrode could be a suitable technique for the detection of DAD from the endocardium of anesthetized cats. In six animals, atrial pacing and graded aortic constriction were performed during MAP recording to assess MAP stability during hemodynamic changes, and in no cases were modifications of the baseline observed. In 11 cats, calcium gluconate (0.5 g) and G-strophanthin (100 micrograms) were administered. Action potential duration at 50% (APD50) and 90% (APD90) repolarization were reduced (from 138 +/- 16 to 122 +/- 18 msec, p less than 0.02, and from 163 +/- 23 to 149 +/- 20 msec, p less than 0.025, respectively). In eight of 11 (73%) animals, DAD were elicited with a mean amplitude of 1.2 +/- 0.4 mV. In 14 cats, the left stellate ganglion was stimulated for 45 seconds. APD50 and APD90 decreased (from 153 +/- 15 to 145 +/- 16 msec, p less than 0.005, and from 176 +/- 18 to 165 +/- 13 msec, p less than 0.001, respectively). DAD were induced in 10 of 14 animals (71%) with a mean amplitude of 1.2 +/- 0.3 mV. These results show that DAD can be induced in vivo by administration of calcium and digitalis and by activation of the cardiac sympathetic nerves. This latter finding further strengthens the existing link between adrenergic activation and ventricular arrhythmogenesis and suggests triggered activity as a likely mechanism.
Two-dimensional echocardiographic features of echinococcosis of the heart and great blood vessels. Clinical and surgical implications.
Authors: Oliver J M , Sotillo J F , Domínguez F J , López de Sá E , Calvo L , Salvador A , Paniagua J M
Published: June 2011

Echocardiographic findings in cardiac echinococcosis have been previously described in isolated cases, but no detailed account of the various echocardiographic aspects and their clinical and surgical implications have ever been reported. We present a retrospective analysis of the two-dimensional echocardiograms of 15 patients with hydatid cysts affecting the heart or great blood vessels. Two-dimensional echocardiogram features were compared with the main clinical syndromes. Surgical confirmation of the echocardiogram findings was available in 12 patients. The cyst sizes ranged from 0.5 to 12 cm in diameter. Eleven patients had single cysts, three patients had two cysts, and one patient had multiple cysts. Cysts were located in the intramyocardial region in nine patients, the pericardial in three, and the paracardial in another three. All intramyocardial cysts protruded into the adjacent cardiac chamber, but in only two patients was there significant tricuspid valvular dysfunction. Pericardial and mediastinal cysts showed compression of cardiac chambers or great blood vessels, and two cysts had ruptured into the descendent thoracic aorta or inferior vena cava. In most patients, two-dimensional echocardiographic images of hydatid cysts were those of a cystic mass having well-defined edges and internal trabeculations corresponding to daughter membranes. However, in four patients, two-dimensional echocardiographic images showed a "solid" mass instead of a cystic mass, and in one patient with the multivesicular variety of echinococcosis, the images showed a large mass with poorly defined edges having a honeycombed appearance causing lysis of the anterior arch of the second and third left ribs. The two-dimensional echocardiographic finding showed good correlation with main clinical syndromes, but anaphylactic reactions occurred in every cyst location. In one patient, postoperative two-dimensional echocardiography showed two small intramyocardial cysts that had not been noticed during preoperative two-dimensional echocardiography or during surgical examination. Pathological examination in the four patients with a solid mass showed replacement of the hydatid liquid by necrotic matter containing membrane residues with a foreign-body inflammatory reaction of a granulomatous type. In conclusion, two-dimensional echocardiography is a very useful tool for diagnosis and management of patients with cardiac echinococcosis, but the great diversity of findings regarding number, size, location, and appearance of cysts must be borne in mind to interpret correctly the two-dimensional echocardiograms.
Transcatheter closure of ventricular septal defects.
Authors: Lock J E , Block P C , McKay R G , Baim D S , Keane J F
Published: June 2011

Between January and October, 1987, we attempted percutaneous transcatheter closure of seven ventricular septal defects (VSD) in six patients; none of the patients was a candidate for operative management. Patients' ages ranged from 8 months to 82 years (6.0-70 kg); diagnoses included postinfarction VSD (n = 4), congenital VSD (n = 1), and postoperative congenital VSD (n = 2). Indications for VSD closure were shock or respiratory failure (n = 5) or multiple episodes of endocarditis (n = 1). Closure was attempted with a Rashkind double umbrella: VSDs were crossed via the left ventricle and a guide wire was advanced to the right heart, snared with a venous catheter, and used to direct a long sheath (and ultimately the double umbrella) across the VSD. We crossed the VSD in all seven attempts, and a 17-mm double umbrella was successfully placed in each VSD. In the first (postinfarction) patient with the largest (12 mm) VSD, the umbrella embolized after 20 seconds to the pulmonary artery (without reducing flow). The other six umbrellas remained in position, either diminishing or abolishing the left-to-right shunts. Postinfarction patients had increasing VSD shunting over the next several days and died; at postmortem, the umbrellas remained well positioned in the septum, with other VSDs present. All three congenital VSDs had absent or diminished shunts after umbrella closure. These preliminary data indicate that transcatheter VSD closure is feasible in selected cases.
Neurohumoral responses to chronic myocardial infarction in rats.
Authors: Hodsman G P , Kohzuki M , Howes L G , Sumithran E , Tsunoda K , Johnston C I
Published: June 2011

In chronic cardiac failure, various neurohumoral mechanisms are activated to sustain blood volume, blood pressure, and organ perfusion. Using the coronary artery ligation model of heart failure in the rat, we have measured changes in vasoactive hormone secretion and related these changes to salt and water status during a 1-month period. When compared with controls, rats with infarction had a marked rise in plasma atrial natriuretic peptide (294 +/- 59 vs. 79 +/- 10 pg/ml, p less than 0.001) although there was no increase in total exchangeable body sodium. Plasma renin activity and plasma aldosterone concentrations were the same for both rats with infarction and controls. Similarly, there were no significant differences in plasma arginine vasopressin, plasma osmolality, or plasma sodium concentration in rats with infarction. Ventricular norepinephrine levels were reduced in animals with infarction (p less than 0.01). Plasma atrial natriuretic peptide levels were raised in this model of chronic left ventricular failure. However, there was no salt retention and little stimulation of the renin-angiotensin-aldosterone system or vasopressin. The results suggest that high circulating atrial natriuretic peptide levels may prevent or limit salt and water retention, either directly or indirectly, by inhibiting the renin-angiotensin-aldosterone system.
Experimental validation of Doppler echocardiographic measurement of volume flow through the stenotic aortic valve.
Authors: Otto C M , Pearlman A S , Gardner C L , Enomoto D M , Togo T , Tsuboi H , Ivey T D
Published: June 2011

In aortic stenosis, evaluation of aortic valve area by the continuity equation assumes that the volume of flow through the stenotic valve can be measured accurately in the left ventricular outflow tract. To test the accuracy of Doppler volume-flow measurement proximal to a stenotic valve, we developed an open-chest canine model in which the native leaflets were sutured together to create variable degrees of acute aortic stenosis. Left ventricular and aortic pressures were measured with micromanometer-tipped catheters. Volume flow was controlled and varied by directing systemic venous return through a calibrated roller pump and back to the right atrium. Because transaortic volume flow will not equal roller pump output when there is coexisting aortic insufficiency (present in 67% of studies), transaortic flow was measured by electromagnetic flowmeter with the flow probe placed around the proximal descending thoracic aorta, just beyond the ligated arch vessels. In 12 adult, mongrel dogs (mean weight, 25 kg), the mean transaortic pressure gradient ranged from 2 to 74 mm Hg, and transaortic volume flow ranged from 0.9 to 3.2 l/min. In four dogs, electromagnetic flow that was measured distal to the valve was accurate compared with volume flow determined by timed collection of total aortic flow into a graduated cylinder (n = 24, r = 0.97, electromagnetic flow = 0.87 Direct +0.13 l/min). In eight subsequent dogs, electromagnetic flow was compared with transaortic cardiac output measured by Doppler echocardiography in the left ventricular outflow tract as circular cross-sectional area [pi(D/2)2] x left ventricular outflow tract velocity-time integral x heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)
Insights into coronary artery disease gained from metabolic imaging.
Authors: Schelbert H R , Buxton D
Published: June 2011

Positron emission tomography offers the possibility of evaluating and quantifying regional myocardial blood flow and metabolism. Used in patients with coronary artery disease, positron emission tomography has demonstrated sustained metabolic activity in regions with reduced blood flow and impaired contractile function, and it thereby enables differentiation between viable myocardium and myocardium that has succumbed to necrosis and scar formation. Viable myocardial regions identified by metabolic rather than functional or blood-flow criteria are frequently observed in patients after an acute coronary event and in patients with stable coronary artery disease. Positron emission tomography reflects either acute myocardial ischemia, "hibernation," as well as "myocardial stunning." Findings from metabolic imaging have proved useful in characterizing more accurately coronary artery disease and its functional consequences. These findings have been found equally useful for clinical management.
Exercise training in patients with severe left ventricular dysfunction. Hemodynamic and metabolic effects.
Authors: Sullivan M J , Higginbotham M B , Cobb F R
Published: June 2011

We studied the effects of exercise training in patients with chronic heart failure attributed to left ventricular dysfunction (ejection fraction, 24 +/- 10%). Twelve ambulatory patients with stable symptoms underwent 4-6 months of conditioning by exercising 4.1 +/- 0.6 hr/wk at a heart rate corresponding to 75% of peak oxygen consumption. Before and after training, patients underwent maximal bicycle exercise testing with direct measurement of central hemodynamic, leg blood flow, and metabolic responses. Exercise training resulted in a decrease in heart rate at rest and submaximal exercise and a 23% increase in peak oxygen consumption from 16.8 +/- 3.8 to 20.6 +/- 4.7 ml/kg/min (p less than 0.01). Heart rate, arterial lactate, and respiratory exchange ratio were unchanged at peak exercise after training. Maximal cardiac output tended to increase from 8.9 +/- 2.7 to 9.9 +/- 3.2 1/min and contributed to improved peak oxygen consumption in some patients, although this change did not reach statistical significance (p = 0.13). Rest and exercise measurements of left ventricular ejection fraction, left ventricular end-diastolic volume, and left ventricular end-systolic volume were unchanged. Right atrial, pulmonary arterial, pulmonary capillary wedge, and systemic arterial pressures were not different after training. Training induced several important peripheral adaptations that contributed to improved exercise performance. At peak exercise, systemic arteriovenous oxygen difference increased from 13.1 +/- 1.4 to 14.6 +/- 2.3 ml/dl (p less than 0.05). This increase was associated with an increase in peak-exercise leg blood flow from 2.5 +/- 0.7 to 3.0 +/- 0.8 l/min (p less than 0.01) and an increase in leg arteriovenous oxygen difference from 14.5 +/- 1.3 to 16.1 +/- 1.9 ml/dl (p = 0.07). Arterial and femoral venous lactate levels were markedly reduced during submaximal exercise after training, even though cardiac output and leg blood flow were unchanged at these workloads. Thus, ambulatory patients with chronic heart failure can achieve a significant training effect from long-term exercise. Peripheral adaptations, including an increase in peak blood flow to the exercising leg, played an important role in improving exercise tolerance.(ABSTRACT TRUNCATED AT 400 WORDS)
Effect of thromboxane and serotonin receptor antagonists on intracoronary platelet deposition in dogs with experimentally stenosed coronary arteries.
Authors: Golino P , Buja L M , Ashton J H , Kulkarni P , Taylor A , Willerson J T
Published: June 2011

We have reported previously that thromboxane A2 (TXA2) and serotonin (5-HT, 5-hydroxytryptamine) are important mediators of cyclic flow variations (CFVs) in a canine model of coronary artery stenosis and endothelial injury. The present study tested the hypothesis that a TXA2 receptor antagonist is more effective in reducing intracoronary platelet deposition at sites of endothelial injury and severe stenosis than a 5-HT2 receptor antagonist. CFVs developed after placing a plastic constrictor around the left anterior descending coronary artery (LAD) in 51 of 56 dogs. Autologous platelets labeled with 111In were injected in 48 animals. Ten control dogs (group 1A) were killed after CFVs were observed for 1 hour at the nadir of coronary blood flow. Five dogs (group 1B) did not develop CFVs after placement of the constrictor. CFVs were abolished with SQ 28668 (2.75 +/- 0.36 mg/kg, group 2) and SQ 29548 (0.45 +/- 0.1 mg/kg, group 3), two different TXA2 and PGH2 receptor antagonists, in eight of 10 and six of seven dogs, respectively. In eight of 10 dogs (group 4), CFVs were abolished with ketanserin (0.66 +/- 0.12 mg/kg), a 5-HT2 receptor antagonist. In group 2, 3, and 4 dogs, the respective drugs were given so that the minimal dose required to abolished CFVs was administered. In six of six dogs (group 5), a higher dose of ketanserin (i.e., 1.5 mg/kg) was used to abolish CFVs. At death, intracoronary platelet deposition was evaluated by calculating the LAD platelet accumulation ratio (111In activity in the LAD/111In activity in the circumflex coronary artery) in 43 dogs and, in 22 dogs, by microscopic examination of the LAD. A marked LAD platelet accumulation ratio was found in group 1A dogs at the stenotic site and in segments immediately distal to it. The LAD platelet accumulation ratio was significantly reduced by both the low and the high doses of ketanserin compared with group 1A dogs (p less than 0.001). However, the two TXA2 receptor antagonists further reduced the LAD platelet accumulation ratio compared with ketanserin-treated animals (p less than 0.01). Microscopic examination confirmed these findings. We conclude that SQ 28668 and SQ 29548, two different TXA2 receptor antagonists, reduce residual intracoronary platelet deposition associated with CFVs in this canine model more effectively than ketanserin, a 5-HT2 receptor antagonist.
Platelets, vasoconstriction, and nitroglycerin during arterial wall injury. A new antithrombotic role for an old drug.
Authors: Lam J Y , Chesebro J H , Fuster V
Published: June 2011

Endothelial injury in vivo is associated with platelet deposition and a localized platelet-dependent vasoconstrictive response. To assess the influence of nitroglycerin on platelets and vasoconstriction, quantitative 111In-labeled platelet deposition (no platelets x 10(6)/cm2) of the injured segment and the degree of angiographic vasoconstriction (percent diameter narrowing proximal and distal to the dilated segment) produced during injury by balloon angioplasty of the common carotid arteries were studied in heparinized normal pigs that were sacrificed immediately after the procedure. In deeply injured (injury extending through the internal elastic lamina) compared with mildly injured (deendothelialization only) arteries, there was both greater platelet deposition (63.8 vs. 6.9, p = 0.04) and more vasoconstriction (30% vs. 19%, p = 0.02). In the presence of deep arterial wall injury, nitroglycerin given intravenously at a dose sufficient to lower mean arterial pressure by 9 +/- 2% significantly decreased both platelet deposition (16.2 vs. 63.8, p less than 0.008) and the vasoconstrictive response (20 vs. 30%, p less than 0.02) relative to control. However, in the presence of mild arterial wall injury, nitroglycerin decreased vasoconstriction relative to control (10% vs. 19%, p less than 0.01) without causing a significant decrease in the already low level of platelet deposition (5.6 vs. 6.9, respectively; p = NS), suggesting a direct smooth muscle relaxant effect of nitroglycerin. This is the first reported in vivo effectiveness of nitroglycerin in the reduction of platelet deposition after deep arterial injury.
Scintigraphic and electrophysiological evidence of canine myocardial sympathetic denervation and reinnervation produced by myocardial infarction or phenol application.
Authors: Minardo J D , Tuli M M , Mock B H , Weiner R E , Pride H P , Wellman H N , Zipes D P
Published: June 2011

Epicardial phenol application or transmural myocardial infarction in dogs produces sympathetic denervation of myocardium apical to the site of the intervention. Because efferent denervation is probably postganglionic, reinnervation most likely occurs but has not been shown. We investigated whether 123I-labeled metaiodobenzylguanidine (MIBG), a norepinephrine analogue taken up by sympathetic nerve terminals, could provide a scintigraphic image that would detect apical sympathetic denervation and possible reinnervation. Dogs underwent MIBG scintigraphic imaging at various times after phenol application or transmural myocardial infarction. The results of MIBG scintigraphy were correlated with electrophysiological responses obtained during ansae subclaviae and norepinephrine stimulation to establish the presence of neural denervation and reinnervation. Apical defects in the MIBG scan, which were associated with either normal perfusion by thallium or a smaller-sized defect, were found consistently in dogs that had apical sympathetic innervation. MIBG scintigraphic images returned to normal after 14 weeks (mean) at a time when reinnervation was shown to have occurred. Thus, the results of MIBG scintigraphy correlated accurately with the presence of denervation and reinnervation established by neuroelectrophysiological testing. Supersensitive refractory period shortening in response to norepinephrine infusion was present after denervation and persisted for more than 3 weeks after scintigraphic and electrophysiological evidence of reinnervation. Conclusions are that 1) MIBG can be used noninvasively to determine the presence of regional myocardial efferent sympathetic denervation and subsequent reinnervation, 2) reinnervation occurs after phenol application or transmural myocardial infarction, and 3) denervation supersensitivity persists even after reinnervation occurs.
The Dickinson W. Richards lecture. New concepts in assessing cardiovascular function.
Authors: Wasserman K
Published: June 2011

The primary role of the heart is to provide energy for the circulatory transport of oxygen (O2) to cells at rates commensurate with their metabolic activity. At rest, even a "sick" heart may be capable of transporting O2 adequately. But during exercise, the increase in O2 required by muscle cells demands that their blood flow be increased. The supply of O2 needed to meet the O2 requirement for muscle mitochondrial high-energy phosphate generation during exercise is a critical function of the circulation. Thus, the adequacy of cardiovascular function can be estimated, noninvasively, from the pattern of O2 uptake in response to an exercise stimulus. While arterial O2 tension (PaO2) is dependent on pulmonary function (except for intracardiac right-to-left shunt), the mass transfer of O2 (VO2) between the cells and lungs depends on pulmonary blood flow (i.e., cardiac output) and O2 concentration difference between the pulmonary arterial and pulmonary venous blood, C(a-v)O2 (Fick principle). Thus, VO2 in the first 15 seconds of exercise can be used to describe the initial increase in pulmonary blood flow and stroke volume, while the subsequent rise in VO2 results from the further increase in VO2 in response to work rate increase are used to detect circulatory disturbances. Also, the rate of CO2 output (VCO2) has been valuable in the assessment of cardiovascular function when related to VO2. Inadequate O2 availability results in anaerobic metabolism, causing increased muscle lactic acid production. At the pH of cell water, most of the hydrogen ions produced with lactate are buffered by bicarbonate. The CO2 generated by the buffering reaction (22 ml for each milliequivalent) causes a net increase in VCO2 relative to VO2 at the work rate at which buffering begins. This provides a useful estimate of the anaerobic threshold. Thus, study of the dynamic coupling of external to cellular respiration during a work rate stimulus provides valuable, direct, and noninvasive information about cardiovascular mechanisms in health and disease.
Dietary salt intake. A determinant of cardiac involvement in essential hypertension.
Authors: Schmieder R E , Messerli F H , Garavaglia G E , Nunez B D
Published: June 2011

Because a given increase in afterload does not consistently produce the same degree of left ventricular hypertrophy, we evaluated several clinical, hemodynamic, and endocrine factors that are prone to modify the adaptation of left ventricular structure in patients with mild essential hypertension (World Health Organization stages I or II). Dietary salt intake assessed by sodium excretion over 24 hours was a powerful determinant of posterior wall thickness (r = 0.64, p less than 0.001), relative wall thickness (r = 0.67, p less than 0.001), and left ventricular mass (r = 0.37, p less than 0.05). In contrast, diastolic pressure, body mass index, hematocrit, and epinephrine were found to be weaker determinants of left ventricular structure (r = 0.31-0.40, p less than 0.05). A stepwise multiple regression analysis revealed that sodium excretion was the strongest predictor for posterior wall thickness (p less than 0.02) and relative wall thickness (p less than 0.05) independent of the other examined variables. These results identify dietary salt intake as a strong determinant of cardiac structural adaptation to a persistent increase in arterial pressure. Consequently, a high salt intake might aggravate and, conversely, dietary salt restriction might prevent (or at least mitigate) the development of left ventricular hypertrophy in patients with essential hypertension.
Intrathoracic spatial location of specified coronary segments on the normal human heart. Applications in quantitative arteriography, assessment of regional risk and contraction, and anatomic display.
Authors: Dodge J T , Brown B G , Bolson E L , Dodge H T
Published: June 2011

The clinically important coronary segmental anatomy has been described in a format useful for quantitative analysis and standardized display. We have determined the intrathoracic location and course of each of the 23 coronary artery segments and branches commonly used for clinical description of disease. Measurements were averaged from perpendicular angiographic view-pairs in 37 patients with normal-sized hearts. Each segment or branch is described by several points along its course; each point is specified in polar coordinates as the radial distance from the principal coronary ostium and by angles about the patient, corresponding to those describing rotation in c-arm radiographic systems. This computer-assisted measurement method is accurate to within +/- 0.2 cm (SD) and +/- 2 degrees in phantom studies. Coronary segment location among a group of normal-sized hearts can be specified to within +/- 1.0 cm (SD). For example, the left anterior descending coronary artery segment at the apex of the heart is 12.2 +/- 1.0 cm from the left coronary ostium, 32 +/- 4 degrees to the left of the anterioposterior axis, and at 46 +/- 7 degrees of caudal angulation. There are several clinically important applications of this new knowledge. First, this anatomic format provides the basis for estimating regional myocardial contraction and the relative size of the myocardial region at risk from a given arterial occlusion. Second, precise knowledge of "normal" segment location greatly simplifies the computation of dimensional correction factors for quantitative arteriography. Third, viewing angles most appropriate for videodensitometric assessment of lesion lumen area may be computed from these data. The theoretical basis and numerical values needed for most of the above estimates are provided. Finally, a computer program has been written to generate a three-dimensional tree-branch vascular model from these anatomic locations. This easily used interactive program aids in teaching coronary angiographic anatomy and, of importance, permits selection of viewing angles that "best" visualize the traditionally difficult parts of the coronary tree.
Differential response to right and left ansae subclaviae stimulation of early afterdepolarizations and ventricular tachycardia induced by cesium in dogs.
Authors: Ben-David J , Zipes D P
Published: June 2011

Early afterdepolarizations (EADs) are depolarizing potentials that occur before complete repolarization. They may be important in the acquired and possibly the idiopathic long QT syndrome and associated ventricular tachycardia (VT). The purpose of these experiments was to study in 20 open-chest dogs the effects of sympathetic stimulation on EADs and VT produced with cesium chloride (84 mg/kg i.v.) alone or combined with left (LAS), right (RAS), or bilateral (BAS) ansae subclaviae stimulation (2 Hz, 4 msec, 2 mA). We compared the EAD amplitude and area as a percentage of monophasic action potential amplitude and area, respectively, recorded simultaneously with contact electrodes from right (RV) and left ventricular (LV) endocardium and recorded the prevalence of VT induction during each intervention. Both LAS and BAS produced left ventricular EADs with larger amplitudes and areas than did RAS or cesium alone. BAS and LAS produced larger EADs recorded from the LV than from the RV. Cesium produced VT in six of 20 dogs, RAS in three of 20, BAS in 12 of 20, and LAS in 16 of 20. Norepinephrine (0.1-1.5 micrograms/kg/min) caused VT in all dogs by producing a dose-related increase in EAD amplitude that was similar in RV and LV, suggesting that the response of RV and LV EADs to catecholamine stimulation was not intrinsically different. During stimulation of left ansae subclaviae at increasing frequencies (1, 2, 4, and 6 Hz), EADs were significantly larger in LV than in RV at all stimulus frequencies, and the amplitude of EADs in both ventricles increased with increasing stimulus frequencies. Based on the increased LV amplitude and area of cesium chloride-induced EADs during LAS and BAS, with EAD amplitude dependent on the frequency of LAS but with an equal RV and LV EAD amplitude during norepinephrine infusion, it is possible that more norepinephrine released into the LV during LAS and BAS compared with RAS causes larger amplitude LV EADs that reach threshold to cause VT more often. Thus, quantitative differences between the effects of left and right stellate ganglia stimulation rather than qualitative differences or imbalance may account for the arrhythmogenic potential of the left stellate ganglion.
Oscillations of conduction, action potential duration, and refractoriness. A mechanism for spontaneous termination of reentrant tachycardias.
Authors: Frame L H , Simson M B
Published: June 2011

The mechanism of cycle length oscillation and its role in spontaneous termination of reentry was studied in an in vitro preparation of canine atrial tissue surrounding the tricuspid orifice. Reentry occurred around a fixed path with incomplete recovery of excitability. Among 18 experiments, there was complete concordance between the occurrence of spontaneous cycle length oscillation and spontaneous terminations; both were observed in 10 experiments and neither in the other eight (p less than 0.001). Local changes in conduction during oscillations resulted from the dependence of both conduction velocity and action potential duration on the preceding local diastolic interval. Interval-dependent changes in action potential duration contributed to the oscillation by altering the next diastolic interval. Because of changes in action potential duration, changes in cycle length were poorly correlated with changes in diastolic interval and, therefore, with local conduction velocity. Complex oscillations resulted from variations in conduction time at multiple sites in the circuit. Oscillations caused most spontaneous terminations. The critical event was an exceptionally long diastolic interval preceding the next-to-last cycle that accelerated local conduction (which tended to shorten the last cycle) and prolonged action potential duration and refractoriness at the site of block. Ninety-two of 99 recordings of spontaneous termination showed evidence of oscillation of conduction and refractoriness causing block.
Percutaneous transluminal coronary angioplasty improves survival in acute myocardial infarction complicated by cardiogenic shock.
Authors: Lee L , Bates E R , Pitt B , Walton J A , Laufer N , O'Neill W W
Published: June 2011

Modest survival benefits have been reported in patients with acute myocardial infarction complicated by cardiogenic shock who were treated with early surgical revascularization or thrombolytic therapy. To determine whether coronary angioplasty improves survival, 87 patients with cardiogenic shock complicating acute myocardial infarction at the University of Michigan, Ann Arbor, Michigan, from 1975 to 1985 were retrospectively analyzed. Patients in group 1 (n = 59) were treated with conventional therapy; patients in group 2 (n = 24) were treated with conventional therapy and angioplasty. Extent of coronary artery disease, infarct location, and incidence of multivessel disease were similar between groups. Hemodynamic variables including cardiac index, mean arterial pressure, and pulmonary capillary wedge pressure were also similar. The 30-day survival was significantly improved for group 2 patients (50% vs. 17%, p = 0.006). Survival in group 2 patients with successful angioplasty was 77% (10 of 13 patients) versus 18% (two of 11 patients) in patients with unsuccessful angioplasty, (p = 0.006). The findings suggest that angioplasty improves survival in cardiogenic shock compared with conventional therapy with survival contingent upon successful reperfusion of the infarct-related artery.