bluuebunny/crossref_metadata_2025 huggingface dataset:
Chronic aortic regurgitation: reassessment of the prognostic value of preoperative left ventricular end-systolic dimension and fractional shortening.
Authors: Daniel W G , Hood W P , Siart A , Hausmann D , Nellessen U , Oelert H , Lichtlen P R
Published: June 2011

The prognostic significance of a preoperative echocardiographic left ventricular end-systolic dimension (ESD) greater than 55 mm and/or fractional shortening (FS) of 25% or less was evaluated retrospectively in 84 patients who had undergone aortic valve replacement for isolated chronic aortic regurgitation due to various causes. Postoperative survival, improvement in symptoms, and echocardiographic evidence of regression of left ventricular dilatation and hypertrophy were compared between patients with a preoperative ESD greater than 55 mm (category 1) and those with an ESD of 55 mm or less (category 2) and between patients with FS of 25% or less (category 3) and those with FS greater than 25% (category 4). Patients in categories 1 and 3 had a higher preoperative left ventricular end-diastolic dimension (EDD) and cross-sectional area than those in categories 2 and 4, respectively, but their preoperative functional impairment (NYHA class) was similar. There were 13 deaths, only two of which (one early, one late) could be attributed to left ventricular dysfunction. In both, FS was 25% or less and in one ESD was greater than 55 mm. There was a weak association without useful positive predictive value between the echocardiographic variables and postoperative death due to all causes. Among 42 patients with a preoperative ESD greater than 55 mm and/or FS of 25% or less, 33 (79%) were alive at a mean follow-up of 29.5 months. Symptoms improved in all categories of survivors, with the postoperative NYHA class being similar between categories 1 and 2 and between categories 3 and 4. Among 48 survivors with high-quality echocardiograms both before and after surgery, EDD fell in all groups but fell to a lesser extent in category 3 than in category 4. Postoperative cross-sectional area fell to the same level in all categories. Follow-up intervals were similar in all categories. We conclude that in patients undergoing aortic valve replacement for chronic aortic regurgitation, a preoperative ESD greater than 55 mm or an FS of 25% or less does not reliably predict early or late death, does not correlate with lack of improvement in symptoms, and does not preclude postoperative regression of left ventricular dilatation and hypertrophy. Thus these echocardiographic criteria alone cannot be used for the timing of surgical intervention in these patients.
Cryothermal mapping of recurrent ventricular tachycardia in man.
Authors: Gallagher J D , Del Rossi A J , Fernandez J , Maranhao V , Strong M D , White M , Gessman L J
Published: June 2011

Intraoperative reversible cryothermal mapping of recurrent ventricular tachycardia was performed in seven patients with left ventricular aneurysms with use of a 0 degrees C ice probe. A single, reproducible cryotermination site was found in each patient. The cryotermination site was uniformly located in an area where local electrograms obtained during ventricular tachycardia showed electrical activation during the diastolic portion of the surface electrocardiogram, and was different than the site of activation coincident with the onset of the QRS complex on the surface electrocardiogram (earliest reactivation site or ERS) by 4.5 +/- 2.7 cm (mean +/- SD) in five of seven patients. Sinus rhythm late potentials were recorded at the cryotermination site in five of six patients and from the ERS in one. In five patients, extensive subendocardial resection including both the ERS and cryotermination sites was performed. In two patients only the cryotermination site was excised. In six survivors, including one in whom only the cryotermination site was excised, ventricular tachycardia could not be induced 2 weeks after surgery and has not recurred during the follow-up period of 7 to 17 months (12 +/- 4.5 months, mean +/- SD). Reversible cryothermal mapping may provide additional important information not obtained by standard electrogram mapping of ventricular tachycardia that may help guide surgical therapy of recurrent ventricular tachycardia.
Effects of nifedipine on systemic and regional oxygen transport and metabolism at rest and during exercise.
Authors: Choong C Y , Roubin G S , Shen W F , Harris P J , Kelly D T
Published: June 2011

In a placebo-controlled, randomized, cross-over, double-blind study of 12 patients with stable exertional angina, we measured at rest and during bicycle exercise the effects of 20 mg of nifedipine administered sublingually on hemodynamics and systemic and regional oxygen extraction and metabolism. Nifedipine decreased systemic vascular resistance by 38% at rest (p less than .001) and by 28% during exercise (p less than .001). Cardiac output increased from 4.6 +/- 0.6 to 6.0 +/- 0.9 liters/min (p less than .001) at rest after nifedipine and from 10.6 +/- 3.7 to 11.8 +/- 3.4 liters/min (p less than .005) during exercise. After nifedipine, the arterial-mixed venous O2 content difference decreased from 4.7 +/- 0.6 to 3.5 +/- 0.5 ml/100 ml (p less than .001) at rest and from 10.5 +/- 1.7 to 8.8 +/- 1.6 ml/100 ml (p less than .001) during exercise. After nifedipine the arterial-iliac venous O2 content difference also decreased at rest, from 5.9 +/- 1.5 to 4.8 +/- 1.7 ml/100 ml (p = .06) but increased during exercise from 13.1 +/- 1.5 to 14.0 +/- 1.8 ml/100 ml (p less than .05). Oxygen consumption was not significantly altered at rest or during exercise. Nifedipine decreased mixed venous carbon dioxide tension (PCO2) during exercise from 53 +/- 3.5 to 50 +/- 4.0 mm Hg (p less than .05) but increased iliac venous PCO2 slightly from 61 +/- 4.6 to 63 +/- 5.2 mm Hg (p less than .01). Exercise pH was not significantly altered, but arterial lactate increased more after nifedipine (2.65 +/- 1.95 mmol/liter placebo, 3.54 +/- 2.74 mmol/liter nifedipine; p less than .05). Thus nifedipine produces similar changes in O2 extraction in mixed venous and iliac venous blood at rest but directionally opposite changes during exercise. The data support the hypothesis that nifedipine does not alter the distribution of cardiac output to the legs at rest, but during dynamic leg exercise reduces the redistribution of cardiac output to the legs. This probably results from the shunting of blood flow away from exercising muscles by the generalized vasodilatation of nifedipine.
Late phase of nitroglycerin-induced coronary vasodilatation blunted by inhibition of prostaglandin synthesis.
Authors: Trimarco B , Cuocolo A , Van Dorne D , Ricciardelli B , Volpe M , De Simone A , Condorelli M
Published: June 2011

In chloralose-anesthetized dogs with the left circumflex coronary artery perfused at constant flow, the effects of increasing doses of indomethacin or naproxen on the coronary and systemic hemodynamic responses to a 5 microgram intracoronary injection of nitroglycerin (NTG) were evaluated. The integrated areas of NTG-induced coronary vasodilatation were reduced after administration of indomethacin or naproxen. The extent of this reduction was increased progressively by augmenting the dose of indomethacin and naproxen up to 1.5 and 7 mg/kg, respectively. We also assessed the extent of cyclooxygenase inhibition induced by indomethacin or naproxen through the radioimmunoassay of thromboxane B2, which reflects thrombin-induced activation of platelet thromboxane A2 production during whole blood clotting. The level of inhibition progressively increased and complete inhibition was attained with 1.5 mg/kg indomethacin and 7 mg/kg naproxen. Further increase in dosage failed to induce further reduction of integrated areas of coronary vasodilatation, and a correlation was found between the extent of the reduction of the integrated areas of coronary vasodilatation and the dose of indomethacin (r = .828, n = 35, p less than .001) or naproxen (r = .729, n = 35, p less than .001). Finally, the NTG-induced maximum fall in coronary perfusion pressure remained unmodified after inhibition of prostaglandin synthesis, but there was a faster return of the perfusion pressure to the basal value.(ABSTRACT TRUNCATED AT 250 WORDS)
Assessment of papillary muscle function in the intact heart.
Authors: Marzilli M , Sabbah H N , Goldstein S , Stein P D
Published: June 2011

A technique is described to localize the anterolateral papillary muscle and to assess its performance in vivo. Using this technique, we measured sequentially the pressure generated within the anterolateral papillary muscle and its changes in length during the cardiac cycle in eight open-chest anesthetized dogs. Pressure within the anterolateral papillary muscle was measured with a 1.6 mm diameter micromanometer probe. Its dimensional changes were measured with ultrasonic crystals. Pressure within the anterolateral papillary muscle exceeded left ventricular pressure throughout the entire cardiac cycle. A difference of 200 +/- 23 mm Hg was present between systolic pressure in the anterolateral papillary muscle and left ventricular systolic pressure (348 +/- 25 vs 149 +/- 6 mm Hg) (p less than .001). Shortening of the anterolateral papillary muscle began 25 +/- 2 msec after the upstroke of the aortic pressure, continued throughout isovolumic relaxation, and was maximal 68 +/- 5 msec after the apex of the aortic incisura. The extent and velocity of shortening of the anterolateral papillary muscle were maximal when pressure within the muscle was lowest. This temporal dissociation between pressure and dimensional changes of the anterolateral papillary muscle appeared to result from cyclic changes of loading imposed on the muscle.
Regional function and perfusion at the lateral border of ischemic myocardium.
Authors: Homans D C , Asinger R , Elsperger K J , Erlien D , Sublett E , Mikell F , Bache R J
Published: June 2011

To determine whether function is depressed in areas of myocardium adjacent to an area of myocardial ischemia, 16 open-chest dogs were studied with both two-dimensional echocardiography and ultrasonic microcrystals. Regional myocardial blood flow was measured with radioactive microspheres during control periods and after coronary arterial ligation. Segments of myocardium adjacent to the area of ischemia were found to have no significant change in transmural blood flow (1.02 +/- 0.38 ml/g/min control vs 0.95 +/- 0.3 ml/g/min after ligation) or subendocardial flow (1.18 +/- 0.41 ml/g/min control vs. 1.19 +/- 0.37 ml/g/min after ligation). Regional function assessed echocardiographically as percent change in segment area was significantly depressed in these normally perfused adjacent areas (69.5 +/- 18.8% control vs 52.5 +/- 19.8% after ligation; p less than .01). There was a significant relationship between proximity to border of infarction and degree of adjacent dysfunction (r = .50, p less than .01 for echocardiography; r = .70, p less than .01 for ultrasonic microcrystals). It is concluded that systolic performance is depressed in nonischemic myocardium directly adjacent to the lateral border of an area of acute myocardial ischemia.
Predictive survival models for resuscitated victims of out-of-hospital cardiac arrest with coronary heart disease.
Authors: Goldstein S , Landis J R , Leighton R , Ritter G , Vasu C M , Wolfe R A , Acheson A , VanderBrug Medendorp S
Published: June 2011

Resuscitated victims of cardiac arrest with coronary heart disease represent a group of patients with an accelerated mortality rate. Among 227 such patients in our follow-up study, 20% had died at 1 year and 50% were dead in slightly over 3 years. Predictors of death were related to use of digitalis, elevated blood urea nitrogen, cerebral vascular accident, previous myocardial infarction, and age. In a subset of 103 patients in whom ambulatory electrocardiographic recordings were available within 3 months of the arrest event, the presence of complexity and high-frequency ventricular premature beats (VPBs) (greater than or equal to 25/hr) were added to the mortality predictors of digitalis and diuretic therapy and elevated blood urea nitrogen. An almost equal number of patients died suddenly and nonsuddenly. Predictors of sudden death were treatment with quinidine and paired VPBs. Occurrence of arrhythmias was an important addition to the previous mortality predictors related to left ventricular dysfunction.
Simultaneous assessment of left ventricular systolic and diastolic dysfunction during pacing-induced ischemia.
Authors: Aroesty J M , McKay R G , Heller G V , Royal H D , Als A V , Grossman W
Published: June 2011

Both systolic and diastolic dysfunction have been described during pacing-induced ischemia, but the temporal sequence of systolic and diastolic impairment has not been established. Accordingly, 22 patients with coronary artery disease were paced at increasing heart rates and studied with simultaneous hemodynamic monitoring, electrocardiographic recording, and radionuclide ventriculography. In addition, with synchronized left ventricular pressure tracings and radionuclide volume curves, three sequential pressure-volume diagrams were constructed for each patient corresponding to baseline, intermediate, and maximum pacing levels. Eleven patients (group I) demonstrated a nonischemic response to pacing tachycardia without chest pain, significant electrocardiographic changes, or significant rise in left ventricular end-diastolic pressure (LVEDP) in the immediate postpacing period. These patients demonstrated a progressive decrease in LVEDP, end-diastolic volume, and end-systolic volume, no change in cardiac output or left ventricular ejection fraction, and a progressive increase in left ventricular diastolic peak filling rate and the end-systolic pressure-volume ratio. Pressure-volume diagrams shifted progressively leftward and slightly downward, suggesting both an increase in contractility and a mild increase in left ventricular distensibility. The remaining 11 patients (group II) exhibited an ischemic response to pacing tachycardia, with each patient experiencing angina pectoris, demonstrating greater than 1 mm ST segment depression on the electrocardiogram, and exhibiting greater than 5 mm Hg rise in LVEDP immediately after pacing. LVEDP, end-diastolic volume, and end-systolic volume in these patients initially decreased and then subsequently increased during angina, with no change in cardiac output but a decrease in ejection fraction. Left ventricular peak diastolic filling rate and the left ventricular end-systolic pressure-volume ratio both increased at the intermediate pacing rate but fell at maximum pacing. Pressure-volume diagrams for these patients shifted leftward initially, then back to the right, during intermediate and peak pacing levels, often with an upward shift in the diastolic pressure-volume relationship. LVEDP in group II was significantly higher than that in group I at the intermediate pacing level with no difference in end-diastolic or end-systolic volumes, suggesting decreased left ventricular distensibility in these patients before the onset of systolic dysfunction at the maximum pacing level.(ABSTRACT TRUNCATED AT 400 WORDS)
Carotid sinus hypersensitivity: evaluation of the vasodepressor component.
Authors: Almquist A , Gornick C , Benson W , Dunnigan A , Benditt D G
Published: June 2011

The basis of the vasodepressor response in patients with carotid sinus hypersensitivity (CSH) is unknown, and prevention of recurrent vasodepressor-induced hypotension in these patients has not been possible. In this study we assessed the effectiveness of atrioventricular sequential pacing and pharmacologic interventions in the prevention of carotid sinus massage (CSM)-induced vasodepressor responses in eight patients with CSH. Maintenance of constant heart rate (80 beats/min) and atrioventricular synchrony (atrioventricular interval 150 msec) with sequential pacing did not significantly alter mean CSM-induced fall in systolic pressure (CSM control, -60 +/- 12 mm Hg vs CSM with atrioventricular sequential pacing, -48 +/- 19 mm Hg). Similarly, neither pharmacologic muscarinic blockade nor combined muscarinic and beta-adrenergic blockade significantly attenuated CSM-induced fall in systolic pressure (CSM with atropine, -43 +/- 16 mm Hg; CSM with atropine plus propranolol, -47 +/- 18 mm Hg; both p = NS vs atrioventricular sequential pacing alone). On the other hand, intravenous norepinephrine and oral ephedrine blunted the CSM-induced drop in systolic pressure (CSM with norepinephrine, -19 +/- 12 mm Hg; CSM with ephedrine, -21 +/- 11 mm Hg; both p less than .01 vs atrioventricular sequential pacing alone). Thus, vasodepressor responses were not prevented by control of heart rate, maintenance of atrioventricular synchrony, pharmacologic muscarinic blockade, or combined muscarinic and beta-adrenergic blockade, but were attenuated by drugs believed to be predominantly alpha-adrenergic agonists. Consequently, atrioventricular sequential pacing alone may be inadequate to prevent hypotension in patients with pronounced vasodepressor responses, whereas administration of vasoconstrictors such as ephedrine may diminish symptoms.
Independence of left ventricular pressure-volume ratio from preload in man early after coronary artery bypass graft surgery.
Authors: Daughters G T , Derby G C , Alderman E L , Schwarzkopf A , Mead C W , Ingels N B , Miller D C
Published: June 2011

The response of the maximum value of the left ventricular pressure-volume ratio to preload augmentation by blood or plasma expanders was studied in 11 patients during the first 24 hr after coronary artery bypass graft surgery. Increasing the mean left atrial pressure from 10 to 15 and 20 mm Hg resulted in no change in the maximum pressure-volume ratio in the group as a whole. In certain individual patients, however, the maximum pressure-volume ratio changed with volume infusion, and these changes were accompanied by simultaneous changes in afterload. The observed changes in pressure-volume ratio were in the same direction as the changes in afterload (systolic pressure), suggesting a dependence of maximum pressure-volume ratio on afterload. These results show that the maximum pressure-volume ratio is independent of preload in the first 24 hr after coronary artery bypass graft surgery with the pericardium open; thus the maximum pressure-volume ratio is a useful index of postoperative left ventricular function when afterload is unchanged. However, because this ratio (a single-point assessment of the pressure-volume relationship) may not be a good estimate of Emax, we recommend a more complete determination of the locus of the "upper left corners" of the pressure-volume loops for measurement of Emax to provide a more accurate indicator of the myocardial contractile state.
Long-term oral administration of amrinone for congestive heart failure: lack of efficacy in a multicenter controlled trial.
Authors: Massie B , Bourassa M , DiBianco R , Hess M , Konstam M , Likoff M , Packer M
Published: June 2011

A number of uncontrolled studies have indicated that oral administration of amrinone, a phosphodiesterase inhibitor with potent positive inotropic effects in experimental preparations, may be beneficial in patients with chronic congestive heart failure. The present multicenter trial was designed to prospectively evaluate clinical response and change in exercise tolerance during 12 weeks of amrinone therapy in a double-blind, placebo-controlled protocol. Ninety-nine patients with NYHA functional class 3 or 4 congestive heart failure on digitalis and diuretics, of whom 31 were also receiving captopril, were enrolled. After baseline clinical assessment and determination of exercise tolerance, radionuclide left ventricular ejection fraction, and roentgenographic cardiothoracic ratio, patients were randomly assigned to receive amrinone or placebo, beginning at 1.5 mg/kg tid and increasing to a maximum dosage of 200 mg tid. After 12 weeks of therapy or at the last blinded evaluation in patients who did not complete this protocol, there were no significant differences from baseline values between treatment with amrinone or placebo with regard to symptoms, NYHA functional class, left ventricular ejection fraction, cardiothoracic ratio, frequency and severity of ventricular ectopy, or mortality. Exercise tolerance improved significantly from baseline by 37 +/- 10% (mean 163 sec) in patients on amrinone and 35 +/- 11% (mean 149 sec) in patients on placebo, but there was no significant difference between treatments. Adverse reactions were significantly more frequent and more severe on amrinone, occurring in 83% of patients and necessitating withdrawal in 34%.(ABSTRACT TRUNCATED AT 250 WORDS)
Dose requirements and hemodynamic effects of transdermal nitroglycerin compared with placebo in patients with congestive heart failure.
Authors: Jordan R A , Seith L , Henry D A , Wilen M M , Franciosa J A
Published: June 2011

The dose requirements and duration of effect of transdermal nitroglycerin in patients with heart failure are not clearly established. In a first series of eight patients with chronic heart failure we gave transdermal nitroglycerin in incremental doses until pulmonary capillary wedge pressure fell at least 30% within 4 hr in three consecutive patients. Thus we found that a single dose of 60 mg/24 hr (120 cm2) was the minimal effective dose. Transdermal nitroglycerin or placebo was then given as a single application of 60 mg/24 hr in random double-blind fashion to 15 additional patients with heart failure (eight received transdermal nitroglycerin and seven received placebo), and hemodynamics were monitored for up to 24 hr. After administration of transdermal nitroglycerin, the control pulmonary capillary wedge pressure of 22 +/- 7 mm Hg fell by 6 +/- 6 mm Hg at 2 hr (p less than .05) and reached maximal reduction of 8 +/- 6 mm Hg (p less than .01) at 4 hr. The reduction in wedge pressure remained significant through 12 hr but was no longer statistically significant by 18 hr after administration of the drug. Transdermal nitroglycerin also significantly reduced pulmonary arterial and right atrial pressures as well as pulmonary vascular resistance from 4 through 12 hr but did not affect systemic hemodynamics. No significant hemodynamic changes occurred after administration of placebo. Thus transdermal nitroglycerin is an effective vasodilator in patients with heart failure, but a dose of at least 60 mg/24 hr is needed. Even with this dose, hemodynamic effects do not last beyond 18 hr, suggesting altered absorption or development of tolerance.
Investigation of genesis of gallop sounds in dogs by quantitative phonocardiography and digital frequency analysis.
Authors: Aubert A E , Denys B G , Meno F , Reddy P S
Published: June 2011

Several investigators have noted external gallop sounds to be of higher amplitude than their corresponding internal sounds (S3 and S4). In this study we hoped to determine if S3 and S4 are transmitted in the same manner as S1. In 11 closed-chest dogs, external (apical) and left ventricular pressures and sounds were recorded simultaneously with transducers with identical sensitivity and frequency responses. Volume and pressure overload and positive and negative inotropic drugs were used to generate gallop sounds. Recordings were made in the control state and after the various interventions. S3 and S4 were recorded in 17 experiments each. The amplitude of the external S1 was uniformly higher than that of internal S1 and internal gallop sounds were inconspicuous. With use of Fourier transforms, the gain function was determined by comparing internal to external S1. By inverse transform, the amplitude of the internal gallop sounds was predicted from external sounds. The internal sounds of significant amplitude were predicted in many instances, but the actual recordings showed no conspicuous sounds. The absence of internal gallop sounds of expected amplitude as calculated from the external gallop sounds and the gain function derived from the comparison of internal and external S1 make it very unlikely that external gallop sounds are derived from internal sounds.
Linearity of the Frank-Starling relationship in the intact heart: the concept of preload recruitable stroke work.
Authors: Glower D D , Spratt J A , Snow N D , Kabas J S , Davis J W , Olsen C O , Tyson G S , Sabiston D C , Rankin J S
Published: June 2011

The Frank-Starling relationship generally has been examined with filling pressure as the index of preload, resulting in a curvilinear function that plateaus at higher filling pressures. To investigate this relationship further in the intact heart, 32 dogs were chronically instrumented with left ventricular and pleural micromanometers and with regional (10 dogs) or global (22 dogs) ultrasonic dimension transducers. Seven days after implantation, left ventricular pressure and regional or global dimensions were recorded in the conscious state. After autonomic blockade, preload was varied by vena caval occlusion. Myocardial function was assessed by calculating regional or global stroke work, and preload was measured as end-diastolic segment length or chamber volume. The relationship between stroke work and either end-diastolic segment length or chamber volume (termed the preload recruitable stroke work relationship) was highly linear in every study (mean r = .97) and could be quantified by a slope (MW) and x-intercept (LW). Previous nonlinear relationships between stroke work and filling pressure seemed to reflect the exponential diastolic pressure-volume curve. Over the physiologic range of systolic arterial pressures produced by infusion of nitroprusside or phenylephrine, no significant change was observed in MW or LW in the normal dog. Calcium infusion increased both regional and global MW by 71 +/- 19% and 65 +/- 9%, respectively (p less than .02), with no significant change in LW. To normalize for ventricular geometry and heart rate, stroke work was computed from circumferential stress-strain data and converted to myocardial power output, which was then plotted against end-diastolic circumferential strain. This relationship also was highly linear, and the slope, Mmp (mW/cm3 of myocardium), is proposed as a potential measure of intrinsic myocardial performance independent of loading, geometry, and heart rate.
Pulmonary venous flow pattern--its relationship to cardiac dynamics. A pulsed Doppler echocardiographic study.
Authors: Keren G , Sherez J , Megidish R , Levitt B , Laniado S
Published: June 2011

We studied the physiology of pulmonary venous flow in 13 normal subjects and five patients with atrial rhythm disorders and atrioventricular conduction disturbances with pulsed Doppler and two-dimensional echocardiography. The left atrium, mitral valve, and pulmonary venous ostia were visualized through the apical four-chamber view. Mitral and pulmonary venous flows were obtained by placing the Doppler sample volume at the appropriate orifice. Pulmonary venous flow was biphasic: a rapid filling wave was observed during systole when the mitral valve was closed; a second wave was observed in diastole during the rapid ventricular filling phase of mitral flow, but was significantly delayed. In patients without atrial contraction (atrial fibrillation and sinoatrial standstill), the initial rapid filling was greatly diminished and only the second diastolic wave appeared to contribute to left atrial filling. In patients with high-grade atrioventricular block, each atrial contraction was followed by a surge in flow from the pulmonary veins. These results are consistent with data obtained from invasive measurements in both dogs and man, and confirm the validity of the use of pulsed Doppler echocardiography in the study of pulmonary venous flow. We suggest that pulmonary venous flow is influenced by dynamic changes in left atrial pressure created by contraction and relaxation of the atrium and ventricle. The initial peak in pulmonary venous flow occurs with atrial relaxation simultaneously with the reduction of left atrial pressure, and the second peak occurs with left ventricular relaxation and rapid transmitral filling of the ventricle.
The effect of cardiac hypertrophy on the coronary collateral circulation.
Authors: Harrison D G , Barnes D H , Hiratzka L F , Eastham C L , Kerber R E , Marcus M L
Published: June 2011

We have previously shown that dogs with renal hypertension and left ventricular hypertrophy have larger infarcts (per risk area size) than do control animals. A potential explanation for this is that collateral resistance is higher in these dogs. Paradoxically, previous postmortem studies in human hearts with left ventricular hypertrophy have suggested that coronary collaterals are actually increased in this condition. To test the hypothesis that left ventricular hypertrophy is associated with alterations in coronary collateral resistance, studies were performed in dogs with renal hypertension and left ventricular hypertrophy and in patients with aortic valvular disease at the time of cardiac surgery. With an isolated, adenosine-vasodilated, blood-perfused cardiac preparation, collateral and normal zone pressure-flow relationships were established by means of radioactive microspheres in nine dogs with renal hypertension and left ventricular hypertrophy and in 17 controls. Collateral resistance calculated from these pressure-flow relationships were similar in both groups (4.0 +/- 0.7 in dogs with renal hypertension and left ventricular hypertrophy and 3.9 +/- 0.4 mm Hg/ml/min/100 g in controls). In addition, normal zone resistance was not different between groups (transmural resistances 0.17 +/- 0.01 in controls and 0.18 +/- 0.02 in dogs with renal hypertension and left ventricular hypertrophy. In five patients with aortic valve disease, left ventricular hypertrophy, and normal coronary arteries and in six patients without left ventricular hypertrophy who had normal left anterior descending coronary arteries, a 7 MHz suction-mounted echo transducer was used to monitor systolic wall thickening during transient occlusions of the left anterior descending artery at the time of cardiac surgery. Because noncollateralized myocardium ceases to contract promptly after coronary occlusion, this approach provides an indirect index of collateral perfusion. Twenty seconds after the onset of coronary occlusion, systolic thickening had markedly decreased in both groups (15 +/- 10% of control values in nonhypertrophied hearts and 10 +/- 10% in hearts with left ventricular hypertrophy; p = NS between groups). Thus the severity of contraction abnormality induced during transient coronary occlusion in these two groups of patients was similar, suggesting that the degree of severity of ischemia was comparable between the two groups. We conclude that collateral resistance is not altered by hypertension and left ventricular hypertrophy and that left ventricular hypertrophy in patients is not associated with functional evidence of an enhanced collateral circulation.(ABSTRACT TRUNCATED AT 400 WORDS)
Clinical, angiographic, and electrophysiologic findings in patients with aborted sudden death as compared with patients with sustained ventricular tachycardia after myocardial infarction.
Authors: Stevenson W G , Brugada P , Waldecker B , Zehender M , Wellens H J
Published: June 2011

After the acute phase of myocardial infarction, patients who develop sustained ventricular arrhythmias present with either sudden death or ventricular tachycardia (VT). Although current evidence suggests that VT frequently precedes ventricular fibrillation (VF) in patients presenting with sudden death, the factors resulting in rapid deterioration of VT to VF have not been delineated in humans. To determine whether left ventricular function, coronary anatomy, or electrophysiologic characteristics could differentiate patients with sudden death from those with VT without sudden death, we compared results of cardiac angiography and programmed electrical stimulation in 42 patients referred for evaluation of sustained VT or surviving "aborted" sudden death for more than 9 days after myocardial infarction. By univariate analysis there were no differences between patients with sudden death and those with VT in age, time from myocardial infarction to VT or sudden death, ejection fraction (0.31 +/- 0.12 vs 0.29 +/- 0.09), or the number of patients with a major area of contracting myocardium supplied by an artery with a 50% or greater or a 70% or greater stenosis (84% vs 64% and 68% vs 41%). Thirty-six percent of patients with sudden death but no patient with VT had two separate areas of infarction. During programmed electrical stimulation, a sustained ventricular arrhythmia was initiated in 100% of patients with VT and 73% of patients with sudden death and rapidly produced syncope in 67% of patients with sudden death but in only 5% of those with VT. This difference was due to the more frequent initiation of rapid polymorphic VT or VF (27% of patients) and to the shorter VT cycle length (242 +/- 31 vs 319 +/- 69 msec) when monomorphic VT was induced in the group with sudden death. No difference was found in the number of extrastimuli required for initiation of a sustained ventricular arrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)
Mitral valve replacement combined with myocardial revascularization: early and late results for 300 patients, 1970 to 1983.
Authors: Lytle B W , Cosgrove D M , Gill C C , Stewart R W , Golding L A , Goormastic M , Taylor P C , Loop F D
Published: June 2011

Of 300 consecutive patients undergoing primary operation for mitral valve replacement combined with coronary bypass grafting, 22 (7.3%) died in-hospital. Multivariate testing of preoperative and operative descriptors identified radiographic cardiac enlargement, preoperative paced rhythm or atrial fibrillation, 70% or more left main coronary obstruction, and serum bilirubin of more than 2 mg% as factors associated with an increase in in-hospital mortality. Follow-up of the 278 hospital survivors (mean interval 48 months, range 2 to 165 months) documented survival of 85%, 66%, and 31% and an event-free survival of 65%, 46%, and 21% at 2, 5, and 10 postoperative years, respectively. Cox proportional-hazard regression models of late risk implicated in-hospital ventricular arrhythmias, left ventricular dysfunction, and rheumatic or ischemic causes of mitral valve disease in decreasing long-term survival. In addition, patients with bioprostheses without warfarin anticoagulation had better survival and event-free survival than those with bioprostheses taking warfarin and those with mechanical prostheses with or without warfarin.
Beneficial effects of high-dose diltiazem in patients with persistent effort angina on beta-blockers and nitrates: a randomized, double-blind, placebo-controlled cross-over study.
Authors: Boden W E , Bough E W , Reichman M J , Rich V B , Young P M , Korr K S , Shulman R S
Published: June 2011

The effects of orally administered diltiazem combined with maximally tolerated doses of beta-blockers and nitrates were assessed in 12 patients, who during stress testing exhibited persistent effort angina and continued objective evidence for inducible myocardial ischemia. Patients performed multistage semisupine exercise on a bicycle ergometer during equilibrium-gated radionuclide angiography after consecutive 2 week treatment periods of placebo or diltiazem 90 mg qid (mean dose 340 mg/day) combined with maximally tolerated propranolol (mean dose 178 mg/day) and isosorbide dinitrate (mean dose 137 mg/day). All medications (including diltiazem or placebo) were administered four times daily for the duration of the study. Diltiazem or placebo was administered according to a double-blind design, with randomized cross-over at the end of each 2 week treatment period. The average number of angina attacks decreased during the double-blind cross-over phase of the trial (7 +/- 7 episodes/week at baseline vs 4 +/- 3 on placebo vs 2 +/- 2 on diltiazem; p = .08). Angina pectoris was abolished during peak exercise in eight of 12 patients on diltiazem (p less than .05 vs placebo). Diltiazem increased total exercise duration from 276 +/- 92 to 310 +/- 78 sec (p less than .005 vs baseline). Diltiazem likewise increased the time to onset of angina from 231 +/- 84 sec at baseline to 305 +/- 77 sec (p less than .005), as well as the time to the onset of 1 mm ischemic ST segment depression (p = .01). Diltiazem decreased heart rate at rest, during submaximal workload, and at peak exercise (p less than .05), and decreased systolic blood pressure at peak exercise only (p less than .05). A significant decline in rate-pressure product at submaximal and peak exercise was noted (p less than .05). At any given workload there was significantly less ST segment depression during submaximal (p = .05) and peak exercise (p less than .025).(ABSTRACT TRUNCATED AT 250 WORDS)
Electrocardiographic effects of experimental nontransmural myocardial infarction.
Authors: Mirvis D M , Ingram L , Holly M K , Wilson J L , Ramanathan K B
Published: June 2011

Clinical and experimental data have documented the ability of nontransmural myocardial infarction to produce abnormal Q waves on both the epicardial and body surfaces. We undertook this study to define the anatomic determinants of such Q wave development. Thirty dogs were studied before and after occlusion-reperfusion (26 dogs) or latex embolization (four dogs) of the left circumflex coronary artery. Occlusion was maintained for 60 to 240 min before reperfusion to produce nontransmural lesions of various sizes. Electrocardiographic data were registered from 84 torso electrodes by body surface mapping techniques before and 1 week after infarction. Infarct size was quantitated by computer analysis of heart slices stained with triphenyl tetrazolium chloride. Six dogs did not develop infarction. Of the remaining 24, 10 did and 14 did not develop significant changes in body surface Q wave duration and width. The incidence of Q wave changes was not different in dogs with nontransmural and those with transmural lesions. Infarct size (expressed as a percentage of the left ventricle infarcted), the percentage of endocardium subjacent to infarction, the average depth of necrosis, the percent of the four outer fifths of the ventricular wall infarcted, and the duration of occlusion were significantly (p less than .05) greater in dogs with than in those without Q wave changes. Logistic regression modeling demonstrated that only two anatomic parameters--percentage of left ventricle infarcted and average lesion depth--significantly and independently predicted Q wave development. A model including only these two variables accurately classified all 24 cases.(ABSTRACT TRUNCATED AT 250 WORDS)
Myocardial protection via coronary sinus interventions: superior effects of arterialization compared with intermittent occlusion.
Authors: Zalewski A , Goldberg S , Slysh S , Maroko P R
Published: June 2011

It has been reported that infarct size can be reduced by several interventions, by which arterial blood is delivered retrogradely to the ischemic myocardium through the cardiac veins or alternatively the cardiac venous system is intermittently occluded. Accordingly, we studied several modalities of myocardial protection that used the cardiac venous system and compared them by means of a quantitative technique for measuring infarct size. Thus 73 anesthetized dogs with coronary arterial occlusion were randomized into the following groups: group I (n = 9), 6 hr of occlusion without any intervention; group II (n = 11), venovenous shunt (60 ml/min) to the great cardiac vein; group III (n = 11), arteriovenous shunt to the anterior interventricular vein; group IV (n = 12), high flow arteriovenous shunt to the anterior interventricular vein (60 ml/min); group V (n = 11), arteriovenous shunt to the great cardiac vein (60 ml/min); group VI (n = 10), arteriovenous shunt to the great cardiac vein (60 ml/min) combined with diastolic occlusion of the great cardiac vein; group VII (n = 9), intermittent pressure-controlled occlusion of the great cardiac vein without arterialization. The arteriovenous shunt (groups III to VI) or venovenous shunt (group II) was done by selective catheterization of the anterior interventricular vein or the great cardiac vein, advancing a catheter from the jugular vein through the right atrium and coronary sinus under fluoroscopic control. This catheter was then connected to a cannula located either in the carotid artery (groups III to VI) or in the right atrium (group II). One minute after occlusion, 99mTc-labeled albumin microspheres (8 mCi) were injected into the left atrium for the subsequent assessment of the hypoperfused zone, which is the area at risk for infarction.(ABSTRACT TRUNCATED AT 250 WORDS)
An evaluation of automaticity and triggered activity in the canine heart one to four days after myocardial infarction.
Authors: le Marec H , Dangman K H , Danilo P , Rosen M R
Published: June 2011

Both abnormal automaticity and triggered activity induced by delayed afterdepolarizations have been proposed as the primary mechanism for ventricular tachycardia (VT) occurring in dogs 24 hr after ligation of the left anterior descending coronary artery. Because of this controversy, we studied the effects of ventricular pacing and therapeutic concentrations of lidocaine and ethmozin on sustained rhythmic activity of isolated subendocardial preparations excised from the infarct, and on VT in conscious dogs. There were differences in the sustained rhythmic activity cycle length of isolated preparations and the VT cycle length that were attributable to the absence of sympathetic input in the former and its presence in the latter. In isolated tissues, pacing for 1 or 10 beats reset the sustained rhythmic activity and pacing for 1 min induced overdrive suppression. Lidocaine (5 micrograms/ml) had no effect on sustained rhythmic activity but ethmozin (2 micrograms/ml) suppressed it. Delayed afterdepolarizations occurred but appeared to be induced by pacing or by the hyperpolarization associated with recovery. Although delayed afterdepolarizations were infrequent at 24 hr, their frequency increased with the hyperpolarization of the membrane that occurred at 48 to 96 hr after infarction. Delayed afterdepolarizations also occurred more readily when superfusate temperature was lowered. In conscious dogs, pacing the VT for 1 or 10 beats or 1 min had no effect. Lidocaine (2 to 10 micrograms/ml) did not affect the VT but ethmozin (2 to 5 micrograms/ml) increased VT cycle length significantly. Pacing for 1 min in the presence of ethmozin, but not lidocaine, converted VT to sinus rhythm. Our results suggest that although delayed afterdepolarizations occur at 24 hr after infarction in the standard Harris preparation, they are most readily seen as an accompaniment of hyperpolarization, pacing, or lowering of bath temperature. The predominant rhythm at 24 hr appears to be automatic.
Autoimmune myocarditis induced by Trypanosoma cruzi.
Authors: Acosta A M , Santos-Buch C A
Published: June 2011

Antiheart immune reactions have been reported in patients with Chagas' disease, and we have postulated that the observed cardiac lesions are mediated by autoimmune antiheart reactions elicited by the etiologic agent Trypanosoma cruzi. In this report, BALB/c mice infected with a low inoculum of T. cruzi developed splenic lymphocyte cytotoxicity against normal syngeneic neonatal cardiac myofibers in vitro 150 days after infection, whereas splenic lymphocytes obtained from mice at 15, 45, 90, or 120 days after infection or from matched controls did not. No antiheart antibody or antibody-directed cellular cytotoxicity was observed, nor was there an increase in natural killer cell activity. Hearts from mice studied at 150 days after infection showed mononuclear cell myocarditis with myocytolysis in the absence of intracellular T. cruzi forms. Hearts from the other mice did not exhibit any histologic changes. Other reports from our laboratory have identified a cross-reacting antigen (SRA) shared by T. cruzi and striated muscle. Immunization of BALB/c mice with SRA produced immunopathogenic dynamics similar to those seen with long-term T. cruzi infection. Collectively these data indicate that the cardiac lesions seen in patients with Chagas' disease may be attributed to autoimmune reactions elicited by cross-reacting antigens of T. cruzi and striated muscle.
Characterization of the functional significance of subcritical coronary stenoses with H(2)15O and positron-emission tomography.
Authors: Knabb R M , Fox K A , Sobel B E , Bergmann S R
Published: June 2011

We have previously developed a method employing cardiac positron-emission tomography (PET) with 15O (half-life 2.1 min)-labeled water (H2(15)O) and blood pool subtraction with C15O for assessment of myocardial perfusion. This study was performed to determine whether the method developed permits detection of the differences in blood flow, induced by vasodilator stress, indicative of functionally significant subcritical coronary stenosis despite normal perfusion at rest. Coronary stenoses were induced with a small Teflon cylinder placed in the left anterior descending coronary artery of the closed-chest dog. Regional myocardial blood flow was assessed tomographically with H(2)15O given intravenously and C15O given inhalation. Blood flow distal to the stenoses was normal under conditions of rest. However, significant reductions in the hyperemic response to dipyridamole were detected consistently in regions distal to 50% to 70% diameter stenoses. Flow distal to stenoses more than doubled in absolute terms in response to dipyridamole but was only 43 +/- 9% of the increased flow in normal regions in the same dogs or in corresponding anterior regions in normal dogs. Relative myocardial blood flow measured noninvasively with PET correlated closely with the distribution of radiolabeled microspheres measured in vitro (r = .88). Thus, assessment of myocardial blood flow with H(2)15O and PET in dogs at rest and during vasodilator-induced stress permits detection of physiologically significant coronary stenoses. The procedure should therefore prove useful diagnostically for the detection of coronary insufficiency in patients as well as for the assessment of clinical interventions designed to augment regional perfusion.
Echocardiographically detected dyskinesis, myocardial infarct size, and coronary risk region relationships in reperfused canine myocardium.
Authors: Taylor A L , Kieso R A , Melton J , Hite P , Pandian N G , Kerber R E
Published: June 2011

After permanent coronary artery occlusion, the extent of two-dimensional echocardiographically detected dyskinesis correlates well with infarct size. Reperfusion after coronary artery occlusion decreases infarct size; however, contractile function of myocardium salvaged in this way may remain depressed for several weeks. The purpose of this study was to explore the relationship between echocardiographically detected dyskinesis and infarct size in reperfused myocardium. We hypothesized that after transient coronary artery occlusion, the relationship between dyskinesis and infarct size would be altered because of the prolonged depression of contractile function after reperfusion so that dyskinesis would not predict infarct size. We also wanted to explore two related questions: (1) Does inotropic stimulation of reperfused myocardium result in improved systolic function in segments that are dysfunctional but not necrotic? (2) Does the relationship between infarct size and coronary risk region, which is linear in myocardium subjected to permanent coronary occlusion, remain linear in myocardium subjected to a sequence of occlusion and reperfusion? Thirty-seven sedated dogs with preplaced circumflex occluders underwent 1 or 2 hr of coronary artery occlusion, then 2 or 10 days of reperfusion. The percentage of the left ventricle that was dyskinetic was estimated from short-axis two-dimensional echocardiograms at the chordal and papillary muscle level obtained at control, after 1 or 2 hr of occlusion, after 20 min of reperfusion, and after 2 or 10 days of reperfusion. At 2 or 10 days of reperfusion, echocardiograms were also obtained during infusion of dobutamine. Area at risk was determined from postmortem barium-gelatin angiography and infarct size was determined at pathologic examination. We found a significant linear correlation between infarct size and risk region size in reperfused myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)