Citations

It has previously been demonstrated that predictable changes occur in mitral flow velocities under different loading conditions. The purpose of this study was to relate changes in pulmonary venous and mitral flow velocities during different loading conditions as assessed by transesophageal echocardiography in the operating room. Nineteen patients had measurements of hemodynamics, that is, mitral and pulmonary vein flow velocities during the control situation, a decrease in preload by administration of nitroglycerin, an increase in preload by administration of fluids, and an increase in afterload by infusion of phenylephrine. There was a direct correlation between the changes in the mitral E velocity and the early peak diastolic velocity in the pulmonary vein curves (r = 0.61) as well as a direct correlation between the deceleration time of the mitral and pulmonary venous flow velocities in early diastole (r = 0.84). This indicates that diastolic flow velocity in the pulmonary vein is determined by the same factors that influence the mitral flow velocity curves. A decrease in preload caused a significant reduction in the initial E velocity and prolongation of deceleration time, and an increase in preload caused an increase in E velocity and shortening of deceleration time. An increase in afterload produced a variable effect on the initial E velocity and deceleration time and was dependent on the left ventricular filling pressure. The change in systolic forward flow velocity in the pulmonary vein was directly proportional to the change in cardiac output (r = 0.60). The pulmonary capillary wedge pressure correlated best with the flow velocity reversal in the pulmonary vein at atrial contraction (r = 0.81). Use of pulmonary vein velocities in conjunction with mitral flow velocities can help in understanding left ventricular filling.

To improve the predictive accuracy of the signal-averaged electrocardiogram, we created a linear logistic model for predicting ventricular tachycardia during electrophysiologic testing. This signal-averaged electrocardiographic model was created from data obtained from 214 patients undergoing electrophysiologic testing (70 had ventricular tachycardia during electrophysiologic testing) by using stepwise logistic regression to rank eight clinical and nine signal-averaged electrocardiographic variables. The best predictors were ejection fraction, history of infarction, ventricular ectopic pairs or nonsustained ventricular tachycardia on Holter monitoring, QRS duration after 25-Hz filtering, and root mean square voltage of the terminal 40 msec of the QRS complex after 40- and 80-Hz filtering. Cross validation (a statistical technique that can be used to accurately evaluate how a predictive model will perform on a prospective patient population) was used to validate the model. After cross validation, the model's sensitivity was 91% and specificity was 59% for predicting ventricular tachycardia during electrophysiologic testing. This model compared favorably with established 25-Hz late-potential criteria (QRS duration of more than 110 msec and root mean square voltage of less than 25 microV of the terminal 40 msec of the QRS complex; sensitivity, 64%; specificity, 85%) and with established 40-Hz late-potential criteria (QRS duration of more than 114 msec or root mean square voltage of less than 20 microV of the terminal 40 msec of the QRS complex or duration of the low-amplitude signal less than 40 microV at the terminal QRS complex that is greater than 38 msec; sensitivity, 84%; specificity, 54%).(ABSTRACT TRUNCATED AT 250 WORDS)

The outlook for patients with double-outlet right ventricle has improved since the development of corrective operations. Late arrhythmic deaths after successful procedures have been reported; however, the magnitude remains unknown. This study was undertaken to identify the magnitude of late sudden death and the significant factors associated with it. From 1965 through 1985, 118 patients underwent corrective operation for double-outlet right ventricle; of these, 23 died in the hospital and six were lost to follow-up. The 89 remaining patients (52 male and 37 female) made up the study population. Their mean age (+/- SD) was 10.3 +/- 7.8 years at the time of repair. The mean duration of follow-up was 82 months. Of the 22 late deaths, 16 (73%) were sudden. Eight (50%) of the sudden deaths occurred within 1 year of operation. Cox proportional hazards multivariate analysis revealed the following significant risk factors for late sudden death: older age at the time of operation, perioperative or postoperative ventricular tachyarrhythmias, and third-degree atrioventricular block. Factors not associated with late sudden death included year of operation, sex, type and number of associated cardiac anomalies, preoperative functional class, previous palliative procedures, surgical technique, perioperative or postoperative single premature ventricular contractions, and postoperative left or right bundle branch block with or without fascicular block. We conclude that the incidence of late sudden death after successful surgical repair of double-outlet right ventricle is very high. Complete corrective operation at an early age and aggressive diagnosis and treatment of arrhythmias and conduction defects after operation are warranted.

99mTc-hexakis-2-methoxy-2-methylpropyl-isonitrile (Tc-Sestamibi), a new myocardial perfusion radiopharmaceutical, was injected intravenously in 11 patients within 4 hours of the onset of acute myocardial infarction before treatment with intravenous tissue-type plasminogen activator and 6-14 days later. Five patients with acute myocardial infarction who did not receive intravenous thrombolytic therapy underwent a similar injection of radiopharmaceutical. The absence of redistribution of Tc-Sestamibi permitted imaging with single-photon emission computed tomography up to 6 hours after intravenous injection to assess the distribution of myocardial perfusion at the time of administration. The region of hypoperfused myocardium on the initial images varied widely from 9% to 68% of the left ventricle and was significantly greater in anterior than in inferior infarcts (p less than 0.01). The region of hypoperfused myocardium on the final images varied widely from 0% to 63% of the left ventricle and was also greater in anterior infarcts (p less than 0.01). The final hypoperfused region correlated (r = -0.82) with the late resting ejection fraction and with the late regional wall motion score in the infarct segment for both anterior (r = -0.74) and inferior (r = -0.97) infarcts. There was a significant decrease (-13 +/- 11%, p less than 0.003) in the extent of hypoperfused myocardium between the initial and final studies in the patients who received thrombolytic therapy compared with an insignificant increase (4 +/- 6%, p greater than 0.5) in the patients who did not receive thrombolytic therapy. Tomographic imaging with Tc-Sestamibi permits determination of the amount of hypoperfused myocardium "at risk" in acute myocardial infarction. The change in myocardial perfusion determined by Tc-Sestamibi before and after therapy in acute myocardial infarction is a promising tool for assessing treatment.

The inhibitory effects of the endothelium against ergonovine-induced contraction were examined in isolated porcine coronary arteries under normal conditions and after endothelial regeneration. Endothelium-dependent responses were examined in vitro in normal Yorkshire pigs (n = 16) and in pigs that had undergone balloon endothelium removal of the left anterior descending coronary artery (LAD) 4 weeks before the study (n = 10). The presence of a complete endothelial lining was confirmed histologically. In rings from normal arteries contracted with prostaglandin F2 alpha in the presence of indomethacin and ketanserin (a 5-HT2-serotonergic blocker), ergonovine caused endothelium-dependent relaxations. They were attenuated by rauwolscine (an alpha 2-adrenergic blocker), inhibited by methiothepin (a combined 5-HT1- and 5-HT2-serotonergic blocker) or by pertussis toxin (an inhibitor of several G proteins) and abolished by oxyhemoglobin (a selective inactivator of endothelium-derived relaxing factor). In quiescent rings from normal arteries, ergonovine caused contractions that were inhibited by the presence of the endothelium; this endothelium-dependent inhibition was abolished by oxyhemoglobin. The direct contractions were not affected by prazosin (an alpha 1-adrenergic blocker), rauwolscine, 6-hydroxydopamine (an agent causing chemical sympathetectomy), or diphenhydramine (an H1-histaminergic blocker) but were inhibited by ketanserin. In rings with regenerated endothelium contracted with prostaglandin F2 alpha, the endothelium-dependent relaxations to ergonovine were reduced significantly and were not inhibited by pertussis toxin. In quiescent rings with regenerated endothelium, the endothelium-dependent inhibition of ergonovine-induced contraction was less.(ABSTRACT TRUNCATED AT 250 WORDS)

Studies correlating prosthetic valve gradients determined by continuous wave Doppler echocardiography with gradients obtained by cardiac catheterization have, to date, been limited to patients with mitral and tricuspid prostheses or have compared nonsimultaneous measurements. Simultaneous Doppler and catheter pressure gradients in 36 patients (mean age, 63 +/- 13 years) with 42 prosthetic valves (20 aortic, 20 mitral, one tricuspid, and one pulmonary) were studied. Catheter gradients were obtained using a dual-catheter technique. The simultaneous pressure tracings and Doppler flow velocity profiles were digitized at 10-msec intervals to derive the corresponding maximal and mean gradients. The correlation between the maximal Doppler gradient and the simultaneously measured maximal catheter gradient was 0.94 (SEE = 6), and that between the Doppler gradient and the simultaneously measured mean catheter gradient was 0.96 (SEE = 3). There were no significant differences in correlation between gradients for the 32 mechanical valves (maximal gradients: r = 0.95, SEE = 6; mean gradients: r = 0.96, SEE = 3) and the 10 bioprosthetic valves (maximal gradients: r = 0.89, SEE = 6; mean gradients: r = 0.93, SEE = 3). In patients with mitral prostheses, Doppler gradients correlated well with the corresponding catheter gradients obtained with direct measurement of left atrial pressure (maximal gradients: r = 0.96, SEE = 2; mean gradients: r = 0.97, SEE = 1.2). A close correlation between corresponding Doppler and catheter gradients also was found in patients with aortic prostheses (maximal gradients: r = 0.94, SEE = 6; mean gradients: r = 0.94, SEE = 3). Thus, continuous wave Doppler echocardiography can accurately predict the pressure gradient across prosthetic valves.

The present study examined the protective role of the venous endothelium against aggregating platelets and its modulation by diet. Yorkshire pigs were fed a regular chow (control pigs), 2% high-cholesterol diet (for 10 weeks, cholesterol-fed pigs), and regular chow plus cod-liver oil (30 ml/day for 4 weeks, oil-fed pigs). Endothelium-dependent responses were examined in vitro in rings of femoral veins in the presence of the inhibitor of cyclooxygenase indomethacin. In control pigs, aggregating platelets, serotonin, and ADP caused endothelium-dependent relaxations. The platelet-induced relaxations were attenuated by methiothepin (a combined 5-HT1 and 5-HT2 serotonergic blocker) or apyrase (an ADPase and ATPase) and were abolished by the combination of the two agents. In quiescent rings, platelets caused contractions, which were reduced in the presence of endothelium; the contractions were prevented by ketanserin (a 5-HT2 serotonergic blocker) or methiothepin but not by R 68 070 (a thromboxane A2 receptor blocker) or dazoxiben (a thromboxane-synthetase blocker). In cholesterol-fed pigs, the platelet-induced relaxations were not altered, whereas in oil-fed pigs, the endothelium-dependent relaxations to platelets, serotonin, and ADP were augmented. Platelet-induced contractions were significantly reduced in rings with endothelium from oil-fed pigs, whereas the contractions were comparable in rings without endothelium among the three groups. Endothelium-dependent relaxations in response to the calcium ionophore A23187, direct relaxations in response to sodium nitroprusside, and direct contractions in response to potassium chloride were comparable among the three groups.(ABSTRACT TRUNCATED AT 250 WORDS)

The endothelium releases the powerful vasodilator and antiaggregatory substance, EDRF, both under basal conditions and upon stimulation by a wide variety of agents. Endothelial injury or dysfunction may play an important role in the spasmogenicity of the coronary artery, although other possible alterations related to atherosclerosis should also be considered. Among the possible stimuli, aggregating platelets are important as a source of vasoconstrictor substances. The endothelium may also produce the vasoactive substances EDHF and EDCF(s). Their pathophysiologic significance remains to be determined.

The effect of recombinant hirudin and the dosage of heparin on acute platelet-thrombus deposition during carotid angioplasty in anesthetized pigs was prospectively assessed. Fifty-five animals (mean weight, 33.9 kg) were randomized to one of six heparin dosages: heparin boluses of 35, 50, 100, 150, 200, or 250 units/kg followed by a continuous infusion of 35, 50, 100, 150, 200, or 250 units/kg/hr, respectively. Another five pigs received a bolus of 1 mg/kg hirudin (recombinant desulphatohirudin), a specific thrombin inhibitor, followed by an infusion of 1 mg/kg/hr. Bilateral carotid angioplasty was performed in all pigs 20 minutes after starting the infusion; they were sacrificed 57 +/- 12 minutes after the procedure. Deep medial arterial injury was present in approximately 75% of the dilated segments, and subendothelial injury in the remaining 25%. Mean log of number of platelets and molecules of fibrinogen per centimeter squared of deep injury in segments from all the animals treated with heparin were 4.74 +/- 1.03 and 5.02 +/- 0.64, respectively. A regression analysis showed an inverse correlation of the log of platelet deposition with the heparin group (r = -0.56, p = 0.0001) with administered total units of heparin (r = -0.55, p = 0.0003) and with mean plasma heparin concentration (r = -0.55, p = 0.0004) in deeply injured arteries. Similar inverse relations were obtained for fibrinogen. In contrast, the deposition of platelets and fibrinogen in subendothelial injury was very low and independent of the heparin administered.(ABSTRACT TRUNCATED AT 250 WORDS)

This study examined the effects of dietary supplementation with cod-liver oil on impaired endothelium-dependent relaxations in hypercholesterolemia and in atherosclerosis in porcine coronary arteries. Sixteen male Yorkshire pigs underwent balloon endothelium removal of the left coronary arteries and were fed a 2% high-cholesterol diet for 10 weeks, with or without dietary supplementation of cod-liver oil (30 ml/day) (oil-fed and cholesterol-fed groups, respectively). This model allowed the simultaneous examination of the effects of dietary cod-liver oil on vascular reactivity in hypercholesterolemia alone (right coronary artery) and in atherosclerosis (left coronary artery). After 10 weeks of feeding, the dietary treatment with cod-liver oil caused an increase in plasma levels of eicosapentaenoic acid and a decrease in the plasma levels of arachidonic acid, whereas the treatment had no significant effect on the increases in plasma lipid levels induced by the high-cholesterol feeding. Morphometric analysis showed significant inhibition of coronary atherosclerosis by the treatment. Endothelium-dependent responses were examined in vitro in ring preparations and in bioassay experiments. Endothelium-dependent relaxations to bradykinin, serotonin, and adenosine 5'-diphosphate were larger in both right and left coronary arteries from oil-fed than from cholesterol-fed animals. Aggregating platelets from cholesterol-fed and oil-fed pigs induced comparable, larger endothelium-dependent relaxations in rings from oil-fed than from cholesterol-fed pigs. The contractions induced by serotonin or aggregating platelets were significantly inhibited in rings with endothelium from oil-fed pigs, whereas they were comparable in rings without endothelium in both groups. Relaxations to sodium nitroprusside and contractions to potassium chloride or serotonin were comparable in rings without endothelium in both groups. The bioassay experiments revealed that the release of endothelium-derived relaxing factor in response to bradykinin and the relaxations of vascular smooth muscle to the endothelial factor were greater after the fish-oil diet. These results indicate that dietary supplementation of cod-liver oil delays the impairment of endothelium-dependent relaxations in hypercholesterolemia and in atherosclerosis, partly because of an improved release of endothelium-derived relaxing factor and partly because of an improved relaxation of coronary smooth muscle to the factor.