摘要:

During coronary angioplasty, inflation of the balloon within the coronary artery produces transient arterial occlusion and frequently results in myocardial ischemia. Delivery of oxygenated autologous blood to the myocardium at risk during inflation may help mitigate this ischemia. Accordingly, we investigated the feasibility and safety of infusing blood through the central lumen of a dilatation catheter around the guidewire using both a model in vitro and clinical trials. In the tests in vitro, fresh blood was infused at flow rates up to 120 ml/min. Hemolysis was minimal at flow rates of 60 ml/min or less ('E0.92 + 0.18%), but increased exponentially at higher rates (13.64 ± 2.37% at 120 mllmin, p < .002). A similar pattern was observed for potassium release. Platelet and leukocyte counts did not vary significantly, and, 3-thromboglobulin and muramidase remained at control levels. Although mean erythrocyte volume did not change, erythrocyte histograms and light microscopy demonstrated a subpopulation of red cell fragments averaging 25 to 40 fl in size at higher rates. A randomized, crossover clinical trial was next performed by delivery of blood perfusion at 60 ml/min to 15 patients undergoing coronary angioplasty. Levels of plasma hemoglobin, 3-thromboglobulin, lactate dehydrogenase, and potassium remained constant before and after the perfusion and the control inflations. The maximum pain score was significantly lower with the perfusion inflation (4.1 ± 0.8 vs 6.0 ± 0.9, p < .003). Relative to baseline, the maximum ST segment elevation during the perfusion inflation (0.5 ± 0.3 mm) was nearly one-fourth that during the control inflation (1.9 ± 0.6 mm, p < .02). Thus, myocardial protection with oxygenated autologous blood perfusion at rates of 60 ml/min appears to be a safe and effective technique that may permit increased inflation time and extend the range of coronary angioplasty to include individuals at high risk for the procedure.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

This placebo-controlled, double-blind trial compared the hemodynamic effects of sotalol and quinidine with the use of rest and exercise gated radionuclide angiography. Patients had frequent ventricular premature depolarizations (- 30 VPDs/hour) and depressed cardiac function (mean ejection fraction 43 ± 15%). Resting left ventricular ejection fraction and stroke volume index increased (p < .002, p < .001, respectively) during sotalol therapy, associated with a concomitant fall in heart rate (p < .001). Quinidine also increased mean left ventricular ejection fraction, but less so than did sotalol (p < .05). Quinidine significantly decreased left ventricular end-diastolic (p < .05) and end-systolic (p < .002) volumes, but had no effect on stroke volume index or heart rate. Neither drug affected cardiac index. Quinidine resulted in no symptomatic deterioration in left ventricular function or serious arrhythmia aggravation. In contrast, five patients on sotalol developed either decompensated congestive heart failure (two patients), arrhythmia aggravation (two patients), or hypotension associated with bradyarrhythmia (one patient). These patients had a unique hemodynamic profile that can be used to identify patients likely to have a poor outcome on sotalol. This profile reflected a lack of cardiac reserve, characterized by an inability to increase stroke volume and cardiac output with supine bicycle exercise.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

To determine whether high current strength pacing at the site of origin of ventricular tachycardia (VT) could prevent induction of VT, we studied 11 VTs in 10 patients with chronic coronary artery disease. The left ventricular site of origin of all VT was determined by endocardial catheter mapping. Reproducible VT induction from the right ventricular apex or outflow tract was demonstrated with a pacing current strength equal to twice diastolic threshold (.2.0 mA) with single (two VTs), double (eight VTs), or triple (one VT) extrastimuli following 8 beats of a drive cycle length of 400 to 600 msec. After determination of the baseline VT induction zone (range 10 to 80 msec), repeat induction was attempted while simultaneous pacing was performed during the 8 beat drive train from the left ventricular site of origin with the use of a high current strength (10 mA [two VTs] or 20 mA [nine VTsJ) and from the baseline right ventricular site with a current strength equal to twice diastolic threshold. Extrastimuli were introduced only from the right ventricular site over the same range of coupling intervals that resulted in VT initiation during the baseline state. In five of the 1 1 trials, no VT could be initiated; in one trial, the VT induction zone was decreased from 80 to 10 msec; in three trials, only VT of a different morphology and a distinct (> 4 cm distant) site of origin was initiated; and in two trials, VT of the same morphology was initiated. In four of the five trials in which all VT was prevented by simultaneous pacing with a high current strength at the site of origin, simultaneous pacing at a lower current strength (twice diastolic threshold) at the site of origin (three VTs) or with equally increased current strength (10 to 20 mA) at nonsites of origin (two VTs) did not prevent initiation. We conclude that: (1) high current strength pacing at the site of origin during the drive train can inhibit VT induction with extrastimuli and, (2) successful prevention of VT may depend on the pacing site being the site of origin and the current strength used during pacing.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

In this study we introduce a new concept of systolic myocardial stiffness that extends the Suga-Sagawa maximum ventricular elastance concept to the myocardium. End-systole is defined as the time of maximum systolic myocardial stiffness (max Eav), which we examined for its load independence and sensitivity to changes in the inotropic state and to heart rate. Seven adult mongrel dogs were instrumented with ultrasonic crystals for measurements of long and short axes and left ventricular wall thickness, and a high-fidelity micromanometer was inserted for measurement of left ventricular pressures. Preload and afterload were altered by inferior vena cava occlusion, nitroprusside, angiotensin II, atropine, propranolol, and various combinations with propranolol. End-systolic stressstrain relations (slope: max Eav) were linear in all seven dogs, implying that end-systolic myocardial stiffness is independent of end-systolic stress. Changes in max Eav (for constant preload and afterload) reflected changes in the ejection fraction; max Eav was also insensitive to propranolol and to changes in heart rate over the range from 120 to 180 beats/min. End-systolic pressure-volume relations (ESPVRs), derived analytically from these stress-strain relations, were nonlinear, and estimates of volume at zero stress (Vom) were always positive. On the other hand, ESPVRs obtained on the basis of the Suga-Sagawa maximum ventricular elastance concept, were linear, and volume at zero pressure (VOP) estimated by linear extrapolation was negative in one case. Based on the concept of systolic myocardial stiffness, the slope of the ESPVR varies with end-systolic volume and attains its maximum value (Emax) at zero end-systolic pressure. Normalization of Emax with Vom demonstrated a close relationship to max Eav. Thus both max Eav and Vom and Emax are ideal variables for assessing changes in myocardial contractility when preload and afterload are constant. Furthermore, Vom and max Eav permit development of the entire ejection fraction-afterload relationship for a given preload, thus providing a method for comparing myocardial contractile states between ventricles. Circulation 76, No. 2, 343–356, 1987.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Recently proposed concepts of pericardial surface pressure, as opposed to liquid pressure, have advanced our understanding of the relationship between pericardial and heart chamber pressures. However, the subsequent suggestion that right heart intracavitary pressure equals, or nearly equals, pericardial surface pressure is not strictly consistent with the physiology of pericardial constraint. If right heart pressure equals pericardial surface pressure, then transmural right heart pressure equals zero. Because of the difficulty in measuring pericardial pressure directly in the beating heart we designed an experiment in the recently arrested canine heart in situ to measure pericardial pressure indirectly and to test the hypothesis that right heart transmural pressure is zero under reasonably physiologic, static equilibrium conditions. According to a static equilibrium analysis of the pressures acting across the walls of the heart, at a given volume the change in right heart pressure caused by removing the pericardium is equal to the pericardial pressure when the pericardium is intact. We found that this drop in pressure caused by pericardiectomy did not equal right heart pressure and therefore that right heart transmural pressure does not equal zero.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

According to the thoracic pump model of cardiopulmonary resuscitation (CPR), the heart serves as a passive conduit for blood flow from the pulmonary to the systemic vasculature, necessitating an open mitral valve and anterograde transmitral blood flow during chest compression. To assess the applicability of this model to manual CPR techniques, two-dimensional echocardiograms were recorded from the right chest wall and/or the esophagus in nine dogs (18 to 26 kg) during manual CPR. The aortic valve opened with chest compression and closed with release, while the pulmonary and tricuspid valve leaflets closed with compression and opened during release. The mitral valve remained open during ventilation alone and during abdominal compressions. With the onset of brief, high-velocity (high-impulse) chest compressions, the mitral valve closed rapidly and the left ventricle was deformed, whether compressions were applied to the sternum or the left mid-chest wall. The mitral valve reopened with release of each compression. Left atrial echocardiographic contrast injections confirmed the absence of anterograde transmitral blood flow during high-impulse compression and its presence during release. Failure of mitral leaflet approximation during chest compression was observed only when a very low-velocity, prolonged (low-impulse) compression technique was used, or when regions that did not directly overlie the heart were compressed. Consistent with these observations, simultaneous recordings of the left ventricular and left atrial pressures during high-impulse sternal compressions in five dogs (19 to 25 kg) demonstrated peak and mean left ventriculoatrial pressure gradients of 38.5 ± 4.0 and 13.5 ± 2.9 mm Hg, respectively, and these pressure gradients declined with less impulsive compressions. The observations made during all but low-impulse chest compressions are inconsistent with the thoracic pump model, and support direct cardiac compression as the primary mechanism of forward blood flow with more impulsive manual chest compression techniques.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Single-doses or short-term administration of /3-lactam antibiotics alone or combined with aminoglucoside antibiotics have failed to consistently prevent experimental streptococcal endocarditis induced by high inocula of bacteria poorly susceptible to killing by these antibiotics. The optimal duration of administration of antibiotics for successful prophylaxis under these circumstances has not been established. We therefore tested, in rats with catheter-induced sterile aortic vegetations, the duration of administration of antibiotic necessary to prevent endocarditis induced by bacterial inocula 100 to 10,000 times the 90% infective dose of two tolerant viridans-group streptococci and two Streptococcusfaecalis strains. Multiple-dose regimens of amoxicillin alone or of amoxicillin combined with gentamicin were studied. Against the two viridans group streptococci, successful prophylaxis was achieved with multiple doses of amoxicillin alone given over 24 to 48 hr and by the combination of amoxicillin and gentamicin given for 6 to 24 hr. Against the two S. faecalis strains, multiple-dose regimens with amoxicillin alone failed, but the combination of amoxicillin and gentamicin was successful when administered for 48 to 72 hr. Thus, after challenge with high bacterial inocula, repeated doses of a, f-lactam antibiotic alone were sufficient to prevent viridans streptococcal endocarditis, but multiple doses of a bactericidal combination (,3-lactam plus aminoglucoside), as necessary for the treatment of established endocarditis, were a prerequisite for successful prophylaxis of S. faecalis endocarditis.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Denervation supersensitivity was demonstrated in anesthetized dogs 5 to 10 days after transmural myocardial infarction produced by latex embolization of a diagonal branch of the left anterior descending coronary artery. Sympathetic efferent denervation in noninfarcted myocardium apical to the infarction was demonstrated by a 90% depletion of myocardial norepinephrine content in the apical (45 ± 15 pg norepinephrine/g tissue) vs basal (437 ± 76 pg/g tissue) regions and by the lack of effective refractory period (ERP) shortening during bilateral ansae subclaviae stimulation in 34% of sites apical to the infarction. Supersensitivity in the area apical to the infarction was manifested by an exaggerated shortening of the ERP during both norepinephrine and isoproterenol infusions, with an upward and leftward shift in the dose-response curves in the apical vs basal regions (p < .001). The cellular mechanism for denervation supersensitivity did not involve detectable changes in the, Badrenergic receptor adenylate cyclase system. There was no difference in the density of /3-adrenergic receptors ([1251]-cyanopindolol) in the apical (268.6 ± 22.7 fmol/mg protein) vs the basal (253.5 ± 24.8 fmol/mg protein) regions. Adenylate cyclase activity stimulated by guanosine triphosphate plus isoproterenol was slightly greater in the apical (58.7 ± 17.4%) than in the basal (49.6 ± 10.9%) region, but this difference did not reach statistical significance (p = .068). Muscarinic modulation of fl-receptor coupling (oxotremorine attenuation of guanosine triphosphate plus isoproterenol-stimulated adenylate cyclase activity) also was not significantly different at the apical (31.6 ± 17.5% inhibition) and basal (21.4 ± 20.9% inhibition) sites. These data show that a transmural myocardial infarction produces denervation supersensitivity in areas apical to the infarction, but in this preparation no differences in the total number or a redistribution of, B-adrenergic receptors or adenylate cyclase activity were detected.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

A single suction electrode catheter was used for His bundle electrogram recording, His bundle pacing, and low-energy (20 or 30 J) His bundle ablation in seven dogs. The suction electrode catheter was actively fixed to the atrial endocardium at the His bundle level. Electrophysiologic studies were performed in the control state, immediately after, and late (>40 days) after His bundle ablation and results were correlated with histologic findings in the conduction system. Unipolar His bundle recording and pacing were successfully performed in all dogs with the suction electrode catheter before and after ablation. Complete heart block developed after a single 20 J shock delivered via the suction electrode catheter in all dogs immediately, but reverted to 1: 1 atrioventricular conduction with firstdegree atrioventricular block in two dogs in which one or two additional shocks (20 or 30 J) produced complete heart block. Mean ablation energy per shock was 22 ± 4 J. The mean total delivered energy per dog was 31 ± 20 J. Late electrophysiologic study in all dogs showed persistent complete heart block in five dogs and paroxysmal second-degree or third-degree atrioventricular block in two dogs. Gross examination of the ablation site showed a white plaque above the medial tricuspid leaflet (1.4 to 2.0 cm long and 0.4 to 0.6 cm wide). Microscopically, fibrosis of the penetrating and branching His bundle was seen in all dogs, with minimal atrioventricular node and atrial involvement. Significant proximal right bundle branch fibrosis was observed in the two dogs receiving one or two additional shocks. We conclude that the suction electrode catheter permits repeated His bundle recording, pacing, and ablation with a single catheter. Permanent and safe low-energy ablation of the canine His bundle is feasible. Focal injury localized to the target area in the conduction system can be obtained.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

The mechanisms responsible for malignant ventricular arrhythmias associated reperfusion of ischemic myocardium were delineated with a computerized, three-dimensional system, with simultaneous eight-level transmural recordings from 232 bipolar sites. In six chloraloseanesthetized cats, regional ischemia was induced for 10 min by occlusion of the left anterior descending coronary artery, followed by reperfusion. At 10 min after ischemia, just before reperfusion, ventricular activation time during sinus rhythm was significantly delayed (63 + 8 vs 25 + before ischemia, p < .001). Ventricular tachycardia (VT) occurred within 15 sec after reperfusion in three animals culminated in ventricular fibrillation. In 75% of cases of nonsustained VT, initiation occurred in the subendocardium, at the border of the reperfused zone via a mechanism not involving reentry, as determined by the fact that continuous activation was not apparent and the time from of the sinus beat to the beginning of VT (142 + 14 msec) was not associated with any intervening depolarizations. In the remaining 25% of cases of nonsustained VT, initiation of the VT resulted intramural reentry in the subendocardium adjacent to the site of delayed midmyocardial activation the precedlng sinus beat (total activation time = 151 + 9 msec, p < .001 vs just before reperfusion). This reentrant mechanism was similar to that responsible for the majority of cases of VT ischemia without reperfusion. Maintenance of VT during reperfusion occurred by nonreentrant mechanisms as well as by intramural reentry, with most cases of VT involving both mechanisms. Ventricular tachycardia leading to ventricular fibrillation was initiated in the subendocardium at the border reperfused zone by a nonreentrant mechanism and was maintained by both nonreentrant and mechanisms, at times in combination in the same beat. The coupling interval of the first ectopic VT leading to ventricular fibrillation was not significantly different from that of nonsustained ± 16 vs 189 + 9 msec, p – NS). However, during the transition from VT to ventricular fibrillation, nonreentrant mechanisms arising both in the subendocardium and subepicardium led to very acceleration of the tachycardia to the coupling interval of 92 ± 2 msec, resulting in enhanced functional block and further conduction delay, with the total activation time of the transition exceeding the coupling interval of the tachycardia. This subsequently led to the development multiple small reentrant circuits and multiple simultaneous wavefronts characteristic of ventricular fibrillation. In the cases of nonsustained VT, none demonstrated nonreentrant activation in the epicardium or a cycle length less than 120 msec. Likewise, no rapid nonreentrant activation of the endocardium or development of ventricular fibrillation was demonstrated. Thus, VT during reperfusion of myocardium is most commonly initiated by a nonreentrant mechanism, although intramural reentry contribute. Ventricular fibrillation occurs through a rapid nonreentrant acceleration of the tachycardia. The nature of this nonreentrant excitation remains to be elucidated, but may involve an abnormal of automaticity or triggered activity.

ISSN:0009-7322    

出版商:OVID    

年代:1987

数据来源: OVID