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Background . Experiments were designed to determine the feasibility of sodding an endothelial monolayer within the lumen of a prosthetic conduit applied to the canine coronary circulation. Methods . Autologous endothelial cells were sodded onto the luminal surface of the Permaflow conduit and immediately implanted to bypass the left circumflex coronary artery in adult mongrel dogs (n = 9). Unsodded Permaflow conduits were implanted as controls (n = 8). At 3 weeks, grafts were explanted and examined by scanning electron microscopy and immunostained for canine von Willebrand factor. Results . Sodded grafts contained a confluent endothelial cell layer devoid of adherent thrombus or platelets and stained positively for canine von Willebrand factor. Unsodded grafts contained no endothelium and retained adherent platelets, collagen, and fibrin. Effluent from sodded grafts stimulated with calcium ionophore A23187 caused a significantly greater relaxation of its bioassay ring than effluent from unsodded grafts (60% ± 21% versus 12% ± 5%; n=8, p Conclusions . Sodding of endothelial cells onto a Permaflow coronary artery bypass graft results in a confluent, viable, nonthrombogenic, endothelial monolayer and releases vasodilator substances in response to calcium ionophore A23187. Endothelial sodding may optimize prosthetic grafts.

We have studied 322 patients, 80 years of age or older, who underwent aortic valve replacement between June 1971 and December 1992. Two hundred six patients (64%) have had surgery since the end of 1985. Their mean age was 82.7 years (range 80 to 92 years). One hundred seventy-one (53%) were male and most (86%) were in New York Heart Association class III-IV. Fifty-seven patients (18%) required admission to the coronary care unit before the operation. One hundred seventy-nine patients (56%) underwent an urgent or emergency operation. Known cerebrovascular disease was present in 77 (24% of patients), aortic stenosis in 79%, aortic incompetence in 9%, and combined stenosis and incompetence in 12%. Associated procedures included bypass grafting in 139 (43%), mitral valve replacement/repair in 20 (6%), tricuspid valve repair in 6 (2%), and aortic annular enlargement in 38 (12%). Thirty patients (9.3%) were undergoing reoperation. Hospital mortality was 44 of 322 (13.7%). The median hospital stay was 11 days. On univariate analysis, significant predictors of hospital mortality were female sex, preoperative rest pain, New York Heart Association class III-IV, admission to the coronary care unit, heart failure, mitral valve disease, emergency/urgent operation, chronic obstructive pulmonary disease, bypass grafting, valve size, peripheral vascular disease, and ejection fraction less than 0.35. On multivariate analysis the most important independent predictors of operative mortality were female gender ( p = 0.0001), renal impairment ( p = 0.001), bypass grafting ( p = 0.005), ejection fraction less than 0.35 ( p = 0.01), and chronic obstructive pulmonary disease ( p = 0.028). Age and year of operation did not influence mortality. Five-year survivals for all patients and for operative survivors were 60.2% ± 3.2% and 70.3% ± 3.4%, respectively. On univariate analysis, factors that adversely affected long-term survival were coronary bypass grafting ( p = 0.007), more than two comorbidities ( p = 0.02), male gender ( p = 0.04), and ejection fraction less than 0.35 ( p = 0.04). On multivariate analysis, no factor was consistently significant for long-term survival. At most recent clinical follow-up 85% were angina free and 82% were in class I-II. At least 92% of patients, both at 1 year and at most recent clinical follow-up, believed they had significantly benefited from the operation: Conclusion: Risk factors for aortic valve replacement in octogenarians include female gender, unstable symptoms, poor ejection fraction, renal impairment, and bypass grafting. However, despite a hospital mortality higher than that reported for younger patients, the outlook for operative survivors is excellent, with good relief of symptoms and an expected survival normal for this particular age group. If possible, aortic valve replacement should be done before development of unstable symptoms.(J THORAC CARDIOVASC SURG 1996;111:1026-36)

Coronary vascular intraluminal release of endogenous endothelium-derived substances, such as prostacyclin, may affect downstream cardiac myocyte contractile function. With a “chronic” canine model of endothelialized and deendothelialized internal thoracic artery coronary grafts, we tested the hypothesis that higher basal release of endothelium-derived prostacyclin in internal thoracic artery bypass conduit effluent accelerates functional recovery of postischemic stunned myocardium in the intact circulation. Eleven dogs underwent left internal thoracic artery–left circumflex artery bypass, and the proximal circumflex artery was then ligated. Internal thoracic artery conduit endothelium was denuded by balloon catheter in five dogs before grafting and left intact in six dogs. After 7 days, awake dogs were studied to measure myocardial segment length in the circumflex region with ultrasonic dimension transducers, left ventricular pressure with micromanometers, and circumflex artery flow with an ultrasonic flow probe. Regional contractile function was quantified by the area beneath the linear preload recruitable stroke work relationship at baseline and at intervals after a 15-minute circumflex graft occlusion followed by 3 hours of reperfusion. Heart rate, left ventricular peak pressure, left ventricular end-diastolic pressure, left ventricular peak first derivative of pressure (dP/dt), and circumflex flow were similar (all p not significant) in endothelialized and nonendothelialized dogs during ischemia and reperfusion. Ischemia reduced the preload recruitable stroke work relationship to 44% ± 35% of control values ( p < 0.01) in endothelialized dogs and to 47% ± 18% of control values in nonendothelialized dogs ( p < 0.01) at 15 minutes of reperfusion, indicating a similar ( p not significant) initial degree of injury. During 3 hours of reperfusion, the preload recruitable stroke work relationship returned to 51% ± 17% of control values in endothelialized dogs but to only 35% ± 20% of control values in nonendothelialized dogs ( p < 0.02). Basal intraluminal release of endogenous prostanoids in excised internal thoracic artery conduits was subsequently quantified by ex vivo bioassay of vasoactive properties of conduit effluent on normal coronary artery smooth muscle. Endothelialized conduits induced greater smooth muscle relaxation than did nonendothelialized conduits (67% vs 23%), and this increased relaxation by endothelialized conduits was eliminated by indomethacin, a blocker of prostanoid synthesis. These data indicate that coronary bypass conduit endothelium–derived substances, such as prostacyclin, significantly influence downstream myocardial contractile response to ischemia and reperfusion, independent of alterations in coronary flow in the intact circulation. (J T HORAC CARDIOVASC SURG 1996;111:62-73)

In vitro studies suggest that interventions targeted at myocardial gene regulation of endogenous cytoprotective elements, such as heat-shock protein, may attenuate myocardial ischemic injury. We tested the hypothesis that heat shock-induced expression of myocardial heat-shock protein before ischemia accelerates functional recovery of postischemic stunned myocardium in the intact circulation. Sixteen dogs underwent partial femoral arteriovenous bypass and core temperature was raised to 42° C for 15 minutes in eight dogs (heat-shocked) and maintained at 37° C in eight dogs (nonheat-shocked). After 24 hours dogs were studied to measure myocardial segment length in the circumflex artery region with ultrasonic dimension transducers, left ventricular pressure with a micromanometer, and circumflex coronary flow with an ultrasonic probe. Regional contractile function was quantified by the area beneath the linear preload recruitable stroke work relationship at baseline and at intervals during reperfusion after a 15-minute circumflex artery occlusion followed by 3 hours of reperfusion. Baseline and peak reperfusion hyperemic circumflex flows were 37 ± 9 ml/min and 154 ± 33 ml/min, respectively, in heat-shocked dogs (p < 0.001) and 46 ± 24 ml/min and 171 ± 57 ml/min, respectively, in nonheat-shocked dogs (p < 0.001), with no differences between groups (p = not significant) at any time during reperfusion. Heart rate and left ventricular peak pressure, end-diastolic pressure, and first derivative of left ventricular pressure were similar (all p = not significant) in heat-shocked and nonheat-shocked dogs during ischemia and reperfusion. Before ischemia, preload recruitable stroke work relationship did not differ (p = not significant) in heat-shocked and nonheat-shocked dogs. Ischemia reduced preload recruitable stroke work relationship to 32% ± 8% control (p < 0.001) in heat-shocked dogs and to 19% ± 15% control in nonheat-shocked dogs (p < 0.001) at 15 minutes of reperfusion, indicating a similar (p = not significant) initial degree of injury. During 3 hours of reperfusion, preload recruitable stroke work relationship returned to 80% ± 38% control in heat-shocked dogs but to only 33% ± 13% control in nonheat-shocked dogs (p < 0.0001). Myocardial expression of heat-shock protein, quantified by optical densitometry of Western blots using an antibody specific for HSP70, was greater in heat-shocked than in nonheat-shocked dogs (108 ± 27 versus 71 ± 14 densitometry units, p < 0.005). Exact causal mechanisms remain to be defined, but these data indicate (1) hyperthermic bypass triggers induction of myocardial heat-shock protein and (2) elevated myocardial heat-shock protein is associated with accelerated recovery of stunned myocardium. Promotion of endogenous molecular cytoprotective systems represents a novel and potentially useful strategy for myocardial protection. (J THORAC CARDIOVASC SURG 1995;109:753-64)

So that we could better characterize the effects of left heart assist on right ventricular myocardial muscle mechanics and ventricular mechanical coupling in the injured heart, nine dogs underwent 30 minutes of global cardiac ischemia supported by cardiopulmonary bypass followed by randomly varied levels of left heart assist at 0, 1.0, and 2.0 L/min (0, 37 ± 4, and 74 ± 7 ml/kg per minute). A centrifugal pump with left ventricle-to-aorta bypass was used with the intent to cause left ventricular volume unloading but without complete left ventricular pressure unloading. Right ventricular regional free wall and septal-free wall dimensions were measured by a sonomicrometer and right ventricular pressure by a micromanometer. Pressure and dimension data were acquired over a range of preloads produced by transient vena caval occlusion and at steady state at an initial control point and after ischemia at each level of left heart assist. Right ventricular regional early diastolic function was assessed by percent segmental relaxation during the first third of diastole, end-diastolic compliance by the end-diastolic pressure-dimension relationship, systolic contractile performance by the slope (Mw) and dimension axis intercept (Lw) of the linear preload recruitable stroke work relationship, and right ventricular isovolumic relaxation by the pressure decay time constant. Ischemia reduced Mw of both the free wall (38.3 ± 16.1 to 16.4 ± 4.2 erg · cm−3 · 103, p

To characterize a contemporary, nonhospitalized population with angina pectoris, data were obtained from a geographically diverse cohort of 5,125 outpatients with chronic stable angina cared for by 1,266 primary care physicians between September and November of 1990. Diagnosis was based on history supported by evidence for coronary artery disease (coronary angiography, old myocardial infarction, or an abnormal stress test, either alone or in combination). The mean age of the patients was 69 years and 53% were women. Seventy percent had > 1 associated illness and 64% took > 1 cardiovascular drug. Median angina frequency was approximately 2 episodes/week and increased angina frequency (p < 0.0001) was associated with decreased overall feeling of well-being. Although effort angina was present in 90% of patients, 47% also had rest angina and 35% had mental stress-evoked angina. Female gender (relative risk [RR] 1.09; 95% confidence interval [CI] 1.02 to 1.16), concomitant illness (RR 1.17; CI 1.09 to 1.25), and pharmacotherapy (RR 1.14; CI 1.07 to 1.22) were associated with excess risk for rest angina. Younger age (RR 1.30; CI 1.20 to 1.41), female gender (RR 1.16; CI 1.07 to 1.26), concomitant illness (RR 1.13; CI 1.03 to 1.24), and pharmacotherapy (RR 1.28; CI 1.15 to 1.93) were associated with excess risk for mental stress angina. These data suggest that contemporary outpatients with angina are frequently women and elderly patients with high rates of associated illness, rest, and mental stress-related angina.

To examine late outcome of mitral valve repair in patients with preoperative atrial fibrillation, we reviewed the cases of 323 consecutive patients who underwent mitral valvuloplasty for mitral regurgitation from 1980 to 1991; average age of 215 men and 108 women was 64 years (range 14 to 88 years), and 224 patients (70 %) were in New York Heart Association class III or IV before operation. The main indications for operation were severe mitral regurgitation (76%), coronary artery disease with associated mitral regurgitation (15%), and aortic valve disease (6%). At the time of mitral valve repair, coronary artery bypass grafting was done in 35% of patients, aortic valve replacement was done in 7%, and multiple other procedures were done in 10%. For all patients, the 30-day mortality rate was 2.5% (70% confidence limits 1.6% to 3.4%) and survivorships at 3 and 5 years were 81% and 76%, respectively. Before operation, 216 patients were in sinus rhythm and 97 patients had atrial fibrillation; in the latter group, 11 had recent onset of atrial fibrillation within 3 months preceding mitral valve repair. Comparing patients with preoperative atrial fibrillation to those with sinus rhythm, we found no significant difference in operative mortality (3% versus 1.9%) or 5-year survivorship (74.3% ± 6.3% versus 76.9% ± 4.0%). At late follow-up, atrial fibrillation was present in 5% of patients with preoperative sinus rhythm, 80% of patients with preoperative chronic atrial fibrillation, and 0% of patients with preoperative recent onset atrial fibrillation (p

To determine factors that influence survival and recovery of ventricular function in patients undergoing aortic valve replacement in the current surgical era, baseline risk factors related to outcome were analyzed in 1,012 consecutive patients undergoing aortic valve replacement between 1983 and 1990. Forty-two percent of patients underwent concomitant coronary bypass. Observed survival probabilities (expressed as 30-day/5-year) were 0.97/0.81 overall, 0.99/0.89 for patients aged less than 70 years, and 0.95/0.74 for patients aged 70 years or greater. Advanced age (p < 0.0001), decreased ejection fraction (p < 0.0001), extent of coronary disease (p < 0.006), smaller prosthetic valve (p < 0.03), and advanced New York Heart Association class (p < 0.04) were incremental risk factors for mortality. In patients with preoperative ventricular dysfunction (ejection fraction < or = 0.45), ejection fraction measured 1.4 years after aortic valve replacement improved in 72% and the mean increment in ejection fraction was 0.175 (95% confidence interval, 0.154 to 0.195). The increment in ejection fraction was greater in female patients than in male patients (p < 0.02) and greater in patients without than with coronary disease (p < 0.02). Female sex (p < 0.02) and lesser extent of coronary disease (p < 0.05) were independent predictors of change in ejection fraction. In all patients, early improvement in ejection fraction conveyed an independent subsequent survival benefit (p < 0.0001). The results of aortic valve replacement in the current era are excellent, and the majority of patients with ventricular dysfunction demonstrate significant improvement. Early improvement in ejection fraction, influenced by coexistent coronary artery disease and sex-associated factors, importantly affects subsequent survival.

Background Depression is relatively common in patients with ischemic heart disease (IHD) and is associated with increased risk of mortality and morbidity. However, the mechanisms by which depression adversely affects clinical outcomes of patients with IHD are unknown. This study examined the relationship between depression and myocardial ischemia during mental stress testing and during daily living in patients with stable IHD. Methods and results The Center for Epidemiological Studies-Depression scale (CES-D) was administered to 135 patients with IHD to evaluate depressive symptoms. Radionuclide ventriculography was used to evaluate the occurrence of left ventricular wall motion abnormality (WMA) during mental stress and exercise testing. Forty-eight-hour ambulatory electrocardiography was used to assess myocardial ischemia during daily living. The mean CES-D score was 8.2 (SD 7.4, range 0-47) with a median of 7. Logistic regression models using restricted cubic splines revealed a curvilinear relation among CES-D scores and the probability of ischemia. For patients with CES-D scores ≤19 (81.5% of study population), a 5-point increment in the CES-D score was associated with roughly a 2-fold increase in the likelihood of ischemia during mental stress. For patients with CES-D scores >19, the relation among scores and ischemia during mental stress tended to be inversely related, but the portion of the sample is very small. Similar patterns of results were noted for CES-D scores and ischemia during daily life. Conclusions Patients with mild to moderate depressive symptoms (CES-D scores ≤19) are more likely to exhibit myocardial ischemia during mental stress testing and during daily living. Myocardial ischemia may be one mechanism by which depression increases the risk of mortality and morbidity in patients with IHD. The observed inverse association between higher level of depressive symptoms and ischemic activity needs to be further assessed in large samples.

There is the potential for left ventricular outflow obstruction when small aortic valve bioprostheses are employed in normal-sized or large adults. It has been hoped that bovine pericardial valves would improve hemodynamic performance in the smaller tissue valve sizes.To determine in vivo hemodynamic performance of heterograft aortic valve prostheses, we analyzed echocardiographic data from patients receiving 21- or 23-mm Carpentier-Edwards pericardial, Medtronic Intact, and Carpentier-Edwards porcine bioprostheses. In addition, data from 19-mm Carpentier-Edwards pericardial valves were included for comparison of hemodynamic performance between valve sizes. Doppler echocardiography was performed in 151 patients within 2 weeks of operation. Left ventricular outflow gradient was derived from continuous Doppler measurements of flow velocity, and effective orifice area was calculated by the continuity equation.There were statistically significant differences in hemodynamic performance of different sized prostheses for each valve type (effective orifice area, p0.01; valvular gradient, p0.03). There were, however, no significant differences in effective orifice area or mean gradient for different valve types within each size category.The in vivo hemodynamic performance of these three different aortic valve heterograft bioprostheses is similar. Patient-prosthesis mismatch with heterograft prostheses, as demonstrated by the indexed effective orifice area can be avoided by appropriate sizing and use of annular enlarging techniques when necessary.

Background. As the population ages, an increasing number of patients with previous coronary artery bypass grafting (CABG) will require subsequent aortic valve replacement (AVR). This study examined outcome of AVR after previous CABG and reviewed possible indications for valve replacement at the time of initial myocardial revascularization. Methods. Between March 1975 and December 1994, 145 patients had AVR after previous CABG. Sixty-three patients (43%) had their initial CABG elsewhere. Reoperation for AVR was the second cardiac procedure in 137 patients and the third in 8. Redo CABG with AVR was done in 66 (46%). There were 118 men and 27 women. The mean age at CABG was 64 ± 7.9 years; for AVR this was 71 ± 7.6 years. Results. In 2 young patients accelerated calcific aortic stenosis occurred in the setting of renal failure. Significant aortic stenosis did not appear to be addressed at initial CABG in 3 patients. Transaortic valvular gradient, as measured by cardiac catheterization, increased by 10.4 ± 7.0 mm Hg/y. Twenty-four patients (16.6%) died. The mortality for AVR alone or for AVR + redo-CABG was 15 of 125 patients (12%). For patients having more complicated procedures, the mortality was 9 of 20 (45%). Nine patients (6.2%) suffered a postoperative cerebrovascular accident. Low preoperative ejection fraction measured by echocardiography, sternal reentry problems, complexity of operation, and prolonged cross-clamp and bypass times were significant factors associated with mortality. Age at AVR, interval between operations, the extent of underlying native coronary artery disease, the state of the previously placed bypass conduits, and methods of myocardial preservation were not significant predictors of operative mortality. On multivariate analysis there was only one significant value: prolonged crossclamp time. Conclusions. Aortic valve replacement after previous CABG is associated with a mortality that is higher than that seen after repeat CABG or repeat AVR. It seems prudent, therefore, to use liberal criteria for AVR in those patients who require coronary revascularization and who, at the same time, have mild or moderate aortic valve disease.

To assess the clinical significance of mental stress-induced myocardial ischemia in patients with coronary artery disease (CAD).Cohort study in outpatients in a tertiary care teaching hospital assessed at baseline and followed up for up to 5 years.A total of 126 volunteer patients (112 men, 14 women; mean age, 59 years) with documented CAD and exercise-induced myocardial ischemia.Patients underwent baseline mental stress and exercise testing using radionuclide ventriculography and 48-hour Holter monitoring. Patients were subsequently contacted by mailed questionnaires or telephone to document cardiac events, including death, nonfatal myocardial infarction, and cardiac revascularization procedures. Logistic regression and Cox proportional hazards models were used to examine the prognostic value of the ischemic measures after adjusting for such potential confounding factors as age, baseline left ventricular ejection fraction (LVEF), and history of myocardial infarction.Twenty-eight patients (22%) experienced at least 1 cardiac event. Baseline mental stress-induced ischemia was associated with significantly higher rates of subsequent cardiac events (odds ratio, 2.8; 95% confidence interval [CI], 1.0-7.7; P.05). The LVEF change during mental stress was significantly related to event-free survival (risk ratio [RR], 2.4; 95% CI, 1.12-5.14; P = .02), controlling for age, history of prior myocardial infarction, and baseline LVEF. This relationship remained significant after controlling for electrocardiogram (ECG)-defined ischemia during exercise (RR, 2.2; 95% CI, 1.01-4.81; P.05). The RR for ECG-defined ischemia during exercise testing was 1.9 (95% CI, 0.95-3.96; P = .07) and the RR for ambulatory ECG ischemia was 0.75 (95% CI, 0.35-1.64; P = .47).The presence of mental stress-induced ischemia is associated with significantly higher rates of subsequent fatal and nonfatal cardiac events, independent of age, baseline LVEF, and previous myocardial infarction, and predicted events over and above exercise-induced ischemia. These data suggest that the relationship between psychological stress and adverse cardiac events may be mediated by the occurrence of myocardial ischemia.

PURPOSE To examine the relationship between physical fitness and transient myocardial ischemia (TMI) in the laboratory and during daily life, in a sample of coronary patients with a recent positive exercise test. METHODS 47 patients with coronary disease (CAD) participated in laboratory mental and exercise stress testing and 48-hour outpatient Holter monitoring after being withdrawn from ant-ischemic medications. During laboratory testing, left ventricular performance was assessed by radionuclide ventriculography. Physical fitness was assessed by measurement of oxygen consumption during symptom-limited exercise treadmill testing. RESULTS Higher physical fitness subjects were less likely to exhibit wall-motion abnormalities in response to mental stress (P < .05), and to exercise stress (P < .05) testing. They also had smaller decreases in left ventricular ejection fraction (LVEF) in response to mental stress than less fit subjects (P .056), and exhibited a mean increase in LVEF during exercise, compared to the less fit subjects who exhibited a decrease in LVEF (P < .02). Moreover, higher fit subjects exhibited fewer episodes of TMI (P < .04), for a shorter duration (P < .04), and less total ischemic burden (P < .04) during Holter monitoring. CONCLUSION These findings suggest that within a population of CAD patients, higher levels of physical fitness are associated with less TMI assessed in the laboratory and during routine activities of daily living.

Background The purpose of this study was to determine the correspondence of mental stress–induced ischemia in the laboratory with ambulatory ischemia and to assess the relationship between hemodynamic responses to mental stress and the occurrence of ischemia. Although exercise testing is usually used to elicit myocardial ischemia, ischemia during daily life usually occurs at relatively low heart rates and in the absence of strenuous physical exercise. Mental stress has been shown to trigger ischemic events in the laboratory at lower heart rates but at blood pressures comparable to exercise. We therefore compared the extent to which mental stress and exercise testing identify patients who develop ischemia out of hospital. Methods and Results One hundred thirty-two patients with documented coronary disease and recent evidence of exercise-induced myocardial ischemia underwent 48-hour ambulatory monitoring and radionuclide ventriculography during exercise and mental stress testing. Patients who displayed mental stress–induced ischemia in the laboratory were more likely to exhibit ischemia during daily life ( P P P P Conclusions Among patients with prior positive exercise stress tests, mental stress–induced ischemia, defined by new wall motion abnormalities, predicts daily ischemia independent of exercise-induced ischemia. Exaggerated hemodynamic responses during mental stress testing also identify individuals who are more likely to exhibit myocardial ischemia during daily life and mental stress.

To compare the efficacy of 3-channel ambulatory electrocardiographic monitoring (Holter monitoring) with 2-channel Holter monitoring in the detection of transient myocardial ischemia (TMI), channels CM2, CM5, and modified II were studied. Sixty patients with documented coronary artery disease underwent 48-hour Holter monitoring during their normal daily life, followed by exercise stress testing in the laboratory monitored by means of radionuclide ventriculography and standard 12-lead electrocardiography. Analysis revealed that 3-channel Holter monitoring identified 24 patients with a total of 205 TMI episodes and a total ischemic burden of 371.00 mV-min. By itself, CM2 would have detected only 3 patients (13% of the TMI population), 6 TMI episodes (3% of the total TMI episodes), and a 2.4 mV-min ischemic burden (0.7% of the total ischemic burden). Modified II alone would have identified 17 patients (71% of the TMI population), 160 TMI episodes (78% of the total TMI episodes), and 307.24 mV-min of the ischemic burden (82% of the total ischemic burden). The combination of CM5/modified II identified 23 patients (96% of the TMI population), 201 TMI episodes (98% of the total TMI episodes), and 370.44 mV-min of the ischemic burden (98% of the total ischemic burden). These findings suggest that the electrode placement is more important than the absolute number of channels in the detection of TMI by Holter monitoring.

For many patients with ventricular tachyarrhythmias, the optimal choice of palliative or curative therapies is not yet well established. To refine optimal current treatment strategies, baseline patient characteristics were studied in relation to likelihood of successful outcome in 240 consecutive patients undergoing operation for treatment of ventricular tachyarrhythmias from 1981 to 1991. Indications for operation were sudden cardiac death or inducible ventricular tachyarrhythmias refractory to medical therapy (or both). Treatment was directed endocardial procedures in 77 patients (32%), other cardiac procedures in 57 patients (24%) (coronary artery bypass grafting in 94% and valve procedure in 14%, either with [35%] or without [65%] concomitant implantable cardioverter-defibrillator), and implantable cardioverter-defibrillator alone in 106 patients (44%). Overall 30-day operative mortality was 5% (70% confidence interval, 4%-7%) and 2-year survival was 74% (70% confidence interval, 71%-77%). Overall 2-year freedom from sudden cardiac death was 97% (70% confidence interval, 96%-98%) and was similar (p = not significant) for all treatment modalities. For each treatment modality, multivariate analysis identified independent risk factors for operative mortality and 2-year tachyarrhythmia recurrence, advanced angina and congestive heart failure New York Heart Association classes, and overall mortality. To characterize better the use and benefit of coronary artery bypass grafting, risk factors related to outcome also were identified for patients stratified according to absence (44 patients) or presence (119 patients) of coronary artery disease excluding patients treated by directed endocardial procedures.(ABSTRACT TRUNCATED AT 250 WORDS)

Findings from early studies suggested that the autotransfusion of shed mediastinal blood (ATS) after cardiac surgical procedures led to a reduction in the postoperative banked blood requirements. However, changes in baseline patient characteristics and other blood conservation methods may now negate the benefits of ATS. To determine whether the routine use of ATS is effective in the context of current surgical practice, risk factors related to postoperative banked blood requirements were analyzed in a prospective series of 155 consecutive patients undergoing cardiac operations: 71 patients before and 84 patients after the addition of ATS to an already aggressive standardized blood conservation protocol. The overall mean patient age was 66 ± 11 years; the mean preoperative patient hemoglobin level was 11.8 ± 1.8 g/dL; 48% of the procedures were elective and 12% were reoperations; coronary artery bypass grafting was performed in 73% of the patients and valve repair or replacement in 34%, with no differences between the non-ATS and ATS groups (all, p = not significant). The mean 24-hour postoperative blood loss was 1,278 ± 814 ml in the non-ATS group and 1,721 ± 1,510 mL in the ATS group ( p p = not significant). In the non-ATS group 56% of the patients required postoperative banked blood, compared with only 39% in the ATS group ( p 27 / 38 ) of the non-ATS patients required banked blood, compared with only 34% ( 19 / 56 ) of the ATS patients ( p p = not significant). By multivariate analysis, identified risk factors for postoperative banked blood requirement were advanced preoperative angina class and heart failure class, smaller body surface area, and greater postoperative blood loss (all, p p

Myocardial ischemia has traditionally been related to increased demand, but recent data suggest that intermittent episodes of decreased supply are also important. This article discusses the phenomena underlying the factors that produce spontaneous (non-effort-related) ischemia. These include local arterial phenomena, arterial plaques, endothelial phenomena, neural phenomena, and circadian patterns. The clinical spectrum of myocardial ischemia can be viewed as an interplay among supply, demand, local arterial reactivity, and acute plaque disruption. In addition, neural phenomena and circadian patterns of multiple cardiovascular phenomena combine to make the coronary circulation susceptible to an increased concentration of events in the moring hours, around the time of awakening. With this extension of our understanding of myocardial ischemia, we have reasonable assurance that methods of treatment will advance significantly in the near future.

Objective. —To determine the relative risk of myocardial ischemia triggered by specific emotions during daily life. Design and Setting. —Relative risk was calculated by the recently developed case-crossover method, in which the frequency of a presumed trigger during nonischemic, or control, hours is compared with the trigger's frequency during ischemic, or case, hours. Outpatients at Duke University Medical Center, Durham, NC, underwent 48 hours of ambulatory electrocardiographic (ECG) monitoring with concurrent self-report measures of activities and emotions. Occurrences of negative emotions in the hour before the onset of myocardial ischemia were compared with their usual frequency based on all hours in which ischemia did not occur. Subjects. —From a sample of 132 patients with coronary artery disease and recent evidence of exercise-induced ischemia who underwent 48 hours of ambulatory ECG monitoring, 58 patients exhibited ambulatory ischemia and were included in the analysis. Outcome Measures. —Myocardial ischemia during 48-hour ECG monitoring was defined as horizontal or downsloping ST-segment depression of 1 mm (0.1 mV) or more for 1 minute or longer compared with resting baseline. The ECG data were cross-tabulated with subjects' concurrent diary ratings of 3 negative emotions— tension, sadness, and frustration—and 2 positive emotions—happiness and feeling in control—on a 5-point scale of intensity. Results. —The unadjusted relative risk of occurrence of myocardial ischemia in the hour following high levels of negative emotions was 3.0 (95% confidence interval [CI], 1.5-5.9;P Conclusions. —Mental stress during daily life, including reported feelings of tension, frustration, and sadness, can more than double the risk of myocardial ischemia in the subsequent hour. The clinical significance of mental stress—induced ischemia during daily life needs to be further evaluated.

Although it is clear that mental distress elicits myocardial ischemia, the relationship of mental stress-induced myocardial ischemia (MSI) to prognosis in patients with CAD is unknown. 130 CAD patients with stable angina underwent a series of mental stress and exercise tests using radionuclide ventriculography and standard 12-lead ECG, then were followed for one year, Myocardial ischemia was defined as a new wall-motion abnormality, ejection fraction (EF) decrease g5%. or ST-segment depression ≥0.1 mV from baseline. Cardiac events (CE) were defined as CABG, PTCA, unstable angina admission requiring angiography (UA), nonfatal myocardial infarction (NMI), and cardiac death, of the 130 patients, 50% had both MSI and exercise-induced ischemia (ESI), 18% experienced MSI alone. and 18% had ESI alone. Of the 117 patients achieving one-year follow-up, 20 suffered various CE: 19 had UA, 9 had PTCA, 4 had CABG. 2 had NMI, and 1 died. Logistic regression analyses were performed to examine the possible relationships among age, baseline systolic blood pressure (SBP), baseline EF, MSI, ESI and CE. Results showed that baseline SBP and MSI, but not ESI, were univariable predictors of CE (see Table). Multivariable logistic models were then used, with age, baseline SBP, and baseline EF as covariables, to determine if the addition of either MSI or ESI provided prognostic information in predicting CE. MSI was independently predictive of CE after adjustment for the covariables. Univariable x 2 p Value Age 0.49 0.48 Baseline SBP 5.32 0.02 Baseline EF 0.001 0.97 MSI 4.77 0.03 ESI 0.48 0.49 In conclusion, MSI may have greater prognostic potential than ESI for a specific population of CAD patients.

A massive embolus of the central retinal artery occurred during cardiac catheterization and selective coronary angiography. Anterior chamber paracentesis and coughing resulted in restoration of retinal blood flow and vision within two hours. In two other cases retinal arteriolar embolization was observed in patients who had minimal or no ocular symptoms after cardiac catheterization.

The hemodynamic manifestations of right ventricular dysfunction after ischemic injury depend not only on the severity of injury but also on the degree of coexistent left ventricular dysfunction. A better understanding of right ventricular failure and of optimal therapies has been hindered in part by lack of suitable experimental models of selective and differential ventricular injury. Therefore, we developed a technique of differential ventricular myocardial protection during a period of global cardiac ischemia and examined the effect of such an injury on intrinsic right and left ventricular myocardial function, metabolism, and regional blood flow. Twenty-six dogs were subjected to 30 minutes of ischemia while being supported by cardiopulmonary bypass. During ischemia, right and left ventricular myocardial temperatures were independently varied by selective ventricular endomyocardial thermal regulation. Nine dogs underwent right and left ventricular normothermic ischemia, eight underwent right and left ventricular hypothermic ischemia, and nine underwent right ventricular normothermic and left ventricular hypothermic ischemia. In both ventricles, normothermic ischemia resulted in greater depression of ventricular ability to generate stroke work as a function of end-diastotic dimension (p

To study the accuracy with which long-term prognosis can be predicted in patients with coronary artery disease, prognostic predictions from a data-based multivariable statistical model were compared with predictions from senior clinical cardiologists. Test samples of 100 patients each were selected from a large series of medically treated patients with significant coronary disease. Using detailed case summaries, five senior cardiologists each predicted one- and three-year survival and infarct-free survival probabilities for 100 patients. Fifty patients appeared in multiple samples for assessing interphysician variability. Cox regression models, developed using patients not in the test samples, predicted corresponding outcome probabilities for each test patient. Overall, model predictions correlated better with actual patient outcomes than did the doctors' predictions. For three-year survival, rank correlations were 0.61 (model) and 0.49 (doctors). For three-year infarct-free survival predictions, correlations with outcome were 0.48 (model) and 0.29 (doctors). Comparisons by individual doctor revealed Cox model three-year survival predictions were better than those of four of five doctors (model predictions added significant [p less than 0.05] prognostic information to the doctor's predictions, whereas the converse was not true). For infarct-free survival, the Cox model was superior to all five doctors. Where predictions were made by multiple doctors, the interphysician variability was substantial. In coronary artery disease, statistical models developed from carefully collected data can provide prognostic predictions that are more accurate than predictions of experienced clinicians made from detailed case summaries.

17 preschool children, who had been previously identified as having notable delays or difficulties with development, participated in a remedial nursery school program. Each child spent an average of 9 mo. in the program during which he received individualized instruction and treatment for specific problems. Parental involvement was encouraged, and enrichment activities were emphasized throughout the course of the program. Comparison of participant's pre- and post-program Stanford-Binet IQs showed a significant increase on completion of the remediation.

Whereas the left ventricle has been analyzed extensively, the apparent complexity of right ventricular geometry and contraction has hindered analysis of right ventricular performance by an assessment of instantaneous ventricular dimensions and volume during the cardiac cycle. To address this issue, we examined the temporal and quantitative relation between dynamic right ventricular free wall dimension, rate of pressure development (dP/dt), and pulmonary artery flow in the open-chest dog. Right ventricular free wall chord dimension was recorded by sonomicrometry, right ventricular pressure by micromanometer-tipped catheter, and pulmonary flow by electromagnetic probe. The point of peak positive right ventricular dP/dt closely correlated with the end of isovolumic contraction and initiation of ejection, occurring within 10 +/- 25 msec of initiation of pulmonary flow. Right ventricular dimension at peak positive dP/dt differed from dimension at initiation of chord shortening by less than 3%. Peak negative dP/dt correlated with end ejection, occurring within 10 +/- 25 msec of cessation of pulmonary flow. Right ventricular dimension at peak negative dP/dt differed from minimal dimension by less than 1%. In all dogs, volume ejected from the right ventricular chamber during each cardiac cycle was directly related to the change in right ventricular dimension during the same period (mean r = 0.969). This relationship between right ventricular stroke volume and dimensional change remained linear and was not changed (p = NS) by increases in right or left ventricular afterload induced by constricting the pulmonary artery or descending aorta. Right ventricular stroke work, calculated as the integral of instantaneous right ventricular pressure and dimension, correlated well (mean r = 0.980) with directly measured global right ventricular stroke work over a wide range; it was also not changed (p = NS) by changes in afterload. Accurate assessments of beat-to-beat right ventricular chamber volume and stroke work can be obtained by analysis of dynamic right ventricular chord dimension.

Patient-controlled rapid atrial pacing was used to manage 12 cases of recurrent supraventricular tachycardia refractory to drug therapy. The pacing system consists of an implanted receiver-lead system and an external patient-activated transmitter. In each case, brief periods (5 to 20 seconds) of rapid atrial pacing were effective in terminating the supraventricular tachycardia and resulted in a return to normal sinus rhythm. In three patients, occasional transient episodes of atrial flutter or atrial fibrillation preceded a spontaneous return to normal sinus rhythm. The pacing system was removed in one patient 13 months postoperatively because of persistent pericarditis; one patient died of an unrelated cerebral hemorrhage 13 months postoperatively. Successful management of supraventricular tachycardia has been maintained in the 10 remaining patients for 15 to 36 months (average 26.4). In more than 6,000 patient applications of rapid atrial pacing, there has been only one failure to convert the tachycardia. Successful application of permanent rapid atrial pacing requires (1) prescreening of patients with temporary external rapid atrial pacing to verify susceptibility to conversion of supraventricular tachycardia and absence of anomalous conduction pathways that may permit conduction of rapid pacing rates to the ventricles, and (2) assessment of the patient's ability to use the transmitter properly.

To evaluate the clinical correlates and long-term prognostic significance of silent ischemia during exercise, 1,698 consecutive symptomatic patients with coronary artery disease who had both treadmill testing and cardiac catheterization were studied. These patients were classified into three groups: Group 1 = patients with no exercise ST deviation (n = 856), Group 2 = patients with painless exercise ST deviation (n = 242) and Group 3 = patients with both angina and ST segment deviation during exercise (n = 600).Patients with exercise angina had a history of a longer and more aggressive anginal course (with a greater frequency of angina, with nocturnal episodes and/or a progressive symptom pattern) and more severe coronary artery disease (almost two-thirds had three vessel disease). The 5 year survival rate among the patients with painless ST deviation was similar to that of patients without ST deviation (86% and 88%, respectively) and was significantly better than that of patients with both symptoms and ST deviation (5 year survival rate 73% in patients with exercise-limiting angina). Similar trends were obtained in subgroups defined by the amount of coronary artery disease present.In the total study group of 1,698 patients, silent ischemia on the treadmill was not a benign finding (average annual mortality rate 2.8%) but, compared with symptomatic ischemia, did indicate a subgroup of patients with coronary artery disease who had a less aggressive anginal course, less coronary artery disease and a better prognosis. Thus, silent ischemia during exercise testing in patients with symptomatic coronary artery disease represents an intermediate risk response in the spectrum of exercise-induced ischemia.

Acetylstrophanthidin tolerance tests were carried out in a series of farm pigs in the conscious unrestrained state. Serial testing of these animals showed that the dose to produce cardiac arrhythmias, the duration of the arrhythmias, and the gastrointestinal toxic dose were predictable and stable measures. Three groups of animals were compared: a control group, a sham operated group, and a group who experienced gradual circumflex coronary occlusion and subsequent infarction. The experimental infarction was induced by an Ameroid constrictor. With this technique, it was possible to carry out serial observations of acetylstrophanthidin tolerance during the evolution of the infarction. The toxic dose, the duration and the arrhythmias, and the gastrointestinal intoxicating dose remained unchanged in the control and sham groups. In the 8 animals studied during the evolution of experimental myocardial infarction, the average intoxicating dose was reduced by approximately 1 3 , the arrhythmias lasted twice as long and the usual pattern of cardiac intoxication preceding G1 symptoms was reversed.

A previous report from this institution demonstrated the mechanical superiority of the transthoracic pacemaker over the transvenous, but the former had a much higher morbidity. Since 1968 a transmediastinal extrapleural operation has been used in preference to thoracotomy for permanent epicardial pacing. This report compares 161 patients having 82 transmediastinal (TM) and 100 transvenous (TV) pacemaker electrode implantations. Significant operation-related complications occurred in 17% of the TM group and 19% of the TV group; 1 hospital death occurred in each group. Satisfactory ventricular pacing was established in 100% of the TM patients and 95% of the TV group, including 6% who required electrode repositioning. Pacing was not satisfactory in 5% of the TV group, and conversion to an epicardial system was necessary. Late electrode failure occurred in 24% of the TV group but in only 4% of the TM patients. Erosion or infection of the pacemaker system occurred in 23% of the TV and 7% of the TM patients. The results of this study indicate that the TM method is more reliable than the TV in establishing and maintaining permanent cardiac pacing and that the morbidity in TM as compared with TV implantations is almost the same.

Gradual occlusion of the right coronary artery in the farm pig produces a much lower mortality rate than occlusion of the left anterior descending artery. The rate and extent of collateral vessel development in these 2 arteries after the gradual occlusion of each were compared in the pig using selective coronary cineangiograms. Serial studies were performed over 42 days after placement of an ameroid constrictor on the right coronary artery in 24 pigs (RCA group) and on the left anterior descending artery in 27 pigs (LADA group). Despite similar rates of occlusion, collateral vessels developed earlier in pigs in the RCA group. With partial occlusion collaterals were seen in 75 percent of those in the RCA group and in 33 percent of those in the LADA group. After total occlusion, the contralateral vessel was completely opacified at 1, 2, 3 and 4 weeks in 40, 71, 87 and 100 percent, respectively, of animals studied in the RCA group, compared to 8, 20, 40 and 100 percent of animals in the LADA group. Histologic evidence of myocardial infarction, although present in all animals, was more extensive in animals in the LAPA group. All myocardial infarctions noted were limited to the left ventricle although blood supply to the right ventricle is almost exclusively from the right coronary artery. The difference in the rapidity and extent of collateral vessel development may be related to the dissimilarity in pressure and mass between the right and left ventricles, and it may explain the lower mortality rate, smaller left ventricular infarction and absent right ventricular infarction following occlusion of the right coronary artery.

Roentgen kymography (1,2) and subtraction radiography(3, 4) are of proved value in the diagnosis of cardiovascular diseases. Intercalative chest roentgenography, as designed by Hipona and Greenspan (5), is in essence a combination of both technics. The procedure is accomplished by simply superimposing the systolic image on the photographically reversed diastolic image. On such a composite film, the phasic alteration of the cardiovascular silhouette is qualitatively and quantitatively registered as black or white stripes along the border of the structures. The unwanted nonvascular structures and the vascular structures that have shown no movement are blurred off by subtraction. One distinct difference from the kymogram is that the intercalative roentgenogram provides smooth and natural rather than zigzag borders. The present communication is a report of our experience with the intercalative technic as applied to angiocardiography. Intercalative angiocardiography permits evaluation of the dynamic changes of...

A radionuclide method is described for determination of chamber to chamber cardiac transit times using only an intravenous injection. Using the Digital Autofluoroscope, counts of radioactivity from each square centimeter over the precordium were recorded onto computer tape at 0.23 second intervals after intravenous injection of 10 millicuries of 99mtechnetium pertechnetate. Computer analysis of counts grouped detector units with similar time responses into areas corresponding to discrete cardiac regions. From the resulting indicatordilution curves, appearance, peak and mean transit times were calculated for each cardiac region. Studies were obtained in 10 normal subjects, 14 patients with cardiac septal defects and left to right shunting and 20 patients with valvular stenosis or insufficiency. Among the latter patients, 8 had mitral stenosis and 8 had aortic insufficiency. Patients with a left to right shunt greater than 15 percent consistently demonstrated rapid pulmonary transit of tracer. In addition, specific abnormalities of curve configuration occurred in patients with a shunt greater than 30 percent. Transit times from the right atrium to left ventricle averaged 9.2 ± 1.2 seconds in normal subjects, 13.3 ± 2.2 seconds in patients with mitral stenosis and 14.6 ± 2.8 seconds in patients with aortic insufficiency. Pulmonary mean transit time was 6.6 ± 1.1 seconds in normal patients, 9.2 ± 1.7 seconds in those with mitral stenosis and 11.7 ± 3.1 seconds in those with aortic insufficiency. Pulmonary blood volume was 362 cc/m2 in patients with mitral stenosis and 508 cc/m2 in those with aortic insufficiency. These data suggest that pulmonary mean transit time was prolonged primarily by decreased cardiac output in mitral stenosis and by increased pulmonary blood volume in aortic insufficiency. The simple technique described consistently provided hemodynamic data that appear to be useful for diagnosis and management of cardiac diseases.

Bifurcations of coronary arteries provide a myriad of natural landmarks on the epicardial surface. With biplane coronary cineangiograms, these bifurcations can be located in space and followed in time. By calculating the spatial distances between bifurcations on successive cine frames, multiple epicardial segment lengths and their dynamic changes during the cardiac cycle can be determined. In 5 animals with epicardial metal markers sutured near the coronary bifurcations, epicardial segment lengths measured from opacified bifurcations correlated closely with those obtained from metal markers (SEE = 2.2%). Epicardial segment lengths were not affected by intracoronary injection of contrast medium in the first 5 to 6 cardiac cycles. Biplane coronary Cineangiograms of 11 patients were analyzed. Measurements of individual segment lengths yielded reproducible curves reflecting various phases of ventricular contraction and filling. These curves allowed quantitation and simultaneous comparison of the onset, duration, extent and rate of segment shortening in multiple and selected areas of the heart. In 5 patients, the extent of shorteing was 1 to 19 percent along the septum, 17 to 27 percent on the free wall and 10 to 15 percent at the base of the left ventricle. Mechanical activation of the left ventricle began from the antereoseptal area at the apex and progressed toward the base and the posterior surface. In 5 of 6 patients with coronary artery disease, localized abnormalities of contraction were found in areas of previous myocardial infarction or at regions supplied by the stenotic arteries. The diseased segments showed either systolic lengthening or marked reduction in rate and extent of shortening. The onset of shortening was frequently delayed. In addition to defining the anatomic details of the coronary circulation, biplane coronary cineangiograms provide a wealth of physiologic information regarding the dynamic changes in geometry, dimensions and movements of the heart. As the first step to utilizing this physiologic information, this study has demonstrated the validity, feasibility and clinical usefulness of this technique in assessing regional myocardial performance in man.

Two hundred and five patients who received a total of 247 electrode systems-129 transvenous, 68 transmediastinal and 50 transthoracic-are compared after complete uniform two-year follow-up. The transvenous patients had low hospital morbidity (19%) and short hospital stays (75% ≤ 8 days) but a high incidence of electrode failure by 24 months (38%). The transmediastinal and transthoracic patients had more hospital complications (35% and 34%) and longer periods of hospitalization (57% and 70% > 8 days) but fewer instances of failure by 24 months (16% and 11%). Most transvenous electrode failures were secondary to dislodgement. Transmediastinal right epicardial electrodes had the unique problem of threshold elevation and failure between six and 12 months after implantation as well as a high incidence of sudden death in this same period. Although the high incidence of endocardial electrode instability dictates the need for an alternative approach to permanent pacing, the failure of the transmediastinal approach to significantly alter postoperative morbidity (as compared with transthoracic electrodes) and the incidence of threshold elevation remote from right ventricular implantation suggest that limitation of thoracotomy (via the transmediastinal approach) should not take precedence over left ventricular implantation. Development of electrodes which would provide more permanent low resistance fixation to right ventricular endocardium or epicardium may be necessary before the transthoracic approach can be abandoned.

Twelve patients were reverted from atrial fibrillation to sinus rhythm by the technic of "cardioversion." Brief, light anesthesia was the only drug employed. Under conditions of comparable oxygen consumption cardiac output was measured first in atrial fibrillation and then in sinus rhythm. Eleven patients were studied at rest and five during exercise. Ten of the 11 patients studied at rest showed a reduced arteriovenous oxygen difference with sinus rhythm and seven of the 11 increased cardiac output 0.6 L./min. or greater, an average increase of 34 per cent. All five patients studied at exercise decreased the arteriovenous oxygen difference with sinus rhythm and cardiac output rose 1.1 L./min. or greater in all, an average increase of 17 per cent.

The case of a 17-month-old infant with ventricular tachycardia has been presented. The diagnosis was confirmed by esophageal and right atrial electrocardiography. No cardiac abnormalities were demonstrated by bilane angiocardiography. Quinidine and steroid therapy were effective temporarily for conversion to normal sinus rhythm. Gradually, conversion became more difficult and sustained ventricular tachycardia became refractory to drug therapy. A Lown Cardioverter was employed with a single countershock discharge of 8 to 15 watt seconds (1,000 to 1,370 volts). The shock was electronically timed to occur at the peak of the QRS complex to avoid the vulnerable period of the cardiac cycle (T-wave), wherein the shock may initiate ventricular fibrillation. Normal sinus rhythm was established on five occasions with the administration of a single shock. Following this therapy, the patient remained well and maintained a normal sinus rhythm for ten months while on Quinaglute duratabs® and reserpine.

The electrocardiograms of 538 patients with acute myocardial infarction were searched to identify all instances of atrioventricular (A-V) and intraventricular (I-V) conduction disturbances. Data concerning mode of therapy and clinical complications were obtained by review of the record. These variables were then analyzed for significance in relation to the development of type II A-V block acutely and syncope or sudden death during the first year of follow-up. The most accurate predictor for both these events was the status of A-V conduction in combination with the status of I-V conduction. At highest risk (50%) for type II progression were patients with acute adjacent fascicular block plus P-R prolongation, i.e., left anterior hemiblock plus right bundle-branch block (RBBB), or left bundle-branch block (LBBB), or patients with acute nonadjacent fascicular block, i.e., RBBB plus left posterior hemiblock or alternating bundle-branch block. The nonpaced survivors from this same group, plus any other patients with transient type II progression, were also at high risk (45%) for syncope or sudden death in follow-up. No syncope or sudden death has occurred in seven patients with type II progression discharged with a pacemaker. All other patients were at lower risk for these acute and chronic complications. Thus, the electrocardiogram in acute myocardial infarction can identify a high-risk group for acute type II progression in whom prophylactic pacer insertion may be beneficial. Similarly, the electrocardiogram can identify a high-risk group for syncope or sudden death in follow-up and implicates progression to higher degrees of A-V block as an important pathophysiologic mechanism.The possible role of permanent pacemaker therapy in preventing syncope or sudden death in this high-risk group is also suggested.

Synchronized direct current countershock, “cardioversion,” was used in 70 patients on 94 occasions for reversion of atrial fibrillation or flutter. The method and anesthetic technics are described. A modification of the size and location of the electrode has decreased the incidence of minor discomfort resulting from the procedure and lowered the amount of energy necessary for successful cardioversion. In 90 of 94 episodes, or in 66 of 70 patients, the arrhythmia was restored to sinus rhythm. With a follow-up period of from 1 to 9 months, 52 of 66 patients (79%) remained in sinus rhythm. Fourteen patients (21%) reverted to atrial fibrillation despite multiple cardioversions and maximally tolerated quinidine therapy. Certain factors appear to decrease the chances of maintaining sinus rhythm: duration of fibrillation, type of valvular lesion, functional classification and previous quinidine failure. The advantages anticipated with the restoration of sinus rhythm are discussed. The emergency indication and contraindications are outlined. A broad policy of selection of patients for cardioversion is suggested. The reasons for this approach are the high degree of acute success (94%), the low incidence of complications (5%) and success in maintaining sinus rhythm (79%) for a short follow-up Period.

A case history of a 46-year-old Negro male was presented with rheumatic aortic insufficiency, angina pectoris, and possible subacute bacterial endocarditis. While hospitalized, the patient developed angina pectoris associated with micturition. This was not accompanied by a change in blood pressure, pulse, or increase in respiratory rate. The striking similarity to a description of a case approximately 300 years ago is pointed out and possible mechanisms of this association of angina and micturition are considered.

In the series of 86 patients with the Stokes-Adams syndrome or with symptomatic bradycardia managed with permanently implanted ventricular pacemakers reported on, 35 patients had primary implantation of epicardial leads at thoracotomy and 51 had transvenous endocardial electrodes passed via the jugular venous system for permanent ventricular pacing. The transvenous method of permanent pacemaker implantation appears to be easier to apply with less serious complications and provides the same overall mortality as the transthoracic approach. However, pacemaker failure, both permanent and temporary, is more likely to occur with the transvenous approach. A series of unique complications and findings noted in the transvenous group were thought to be related to the permanent pacing electrode catheter. These included myothought cardial perforation, pericardial friction rubs, intermittent ventricular pacing, and diaphragmatic stimulation. The experience suggests that it is reasonable to employ a transvenous pacemaker initially, recognizing that replacement with a transthoracic pacemaker will be necessary in approximately 16% of the patients and remanipulation of the electrode catheter will be needed in another 13%. Therefore, to undertake transvenous permanent implantation of a pacemaker, one must also be prepared to employ the transthoracic approach in a small but significant number of patients.

Treatment and pretreatment of acetylstrophanthidin-induced ventricular tachycardia was studied in awake pigs. The pharmacologic agents employed were diphenylhydantoin and 2 beta-adrenergic blocking agents, MJ 1999 and propranolol. These agents when administered intravenously at the onset of the arrhythmia significantly shortened the duration of acetylstrophanthidin-induced ventricular tachycardia. Pretreatment with diphenylhydantoin in doses ranging from 5 to 30 mg. per kilogram failed to increase acetylstrophanthidin intoxicating doses. Pretreatment with MJ 1999 and propranolol, likewise, showed no prophylactic effect on acetylstrophanthidin intoxication. Animals pretreated with MJ 1999 had a shorter duration of tachycardia, whereas animals pretreated with propranolol exhibited a high mortality rate. This increased mortality rate from propranolol pretreatment possibly resulted from more profound blockade of beta receptors or severe myocardial depression. These findings indicate that diphenylhydantoin and beta-adrenergic blocking drugs, agents which are effective in the acute therapy of digitalis arrhythmias, do not protect against acetylstrophanthidin toxicity in awake pigs. MJ 1999, previously considered specific for catecholamine-induced arrhythmias, was found to antagonize acetylstrophanthidin toxicity by decreasing the duration of ventricular tachycardia. The high mortality rate with propranolol pretreatment may be relevant to clinical situations where digitalization is undertaken in patients receiving certain beta blocking agents.

Left ventricular performance was studied in 36 patients selected for aorta-to-coronary artery bypass grafts. Derangement of left ventricular function was found to be present in patients with single-vessel disease and symptoms only of angina pectoris. Progressively more severe ventricular impairment was demonstrable in patients with multiple vessel involvement and a history of previous myocardial infarction. The 3 operative deaths occurred in the patients whose ventricular performance was most severely depressed. Early postoperative studies suggest that ventricular performance may be favorably influenced by direct myocardial revascularization.

A seven year experience with pure aortic valvular disease in one hundred fifty-eight patients is reviewed. Three groups (pure aortic stenosis, combined aortic stenosis and insufficiency and pure aortic insufficiency) were contrasted as to etiology, clinical course, hemodynamic and cineangiographic data, and the results of medical versus surgical therapy. The etiologic distribution revealed a congenital origin mainly in pure aortic stenosis (AS), rheumatic in combined aortic stenosis and insufficiency (ASAI), whereas pure aortic insufficiency (AI) had a variable spectrum of etiologies. The clinical course prior to symptoms was one of long compensation to the valvular lesions. The major symptoms were angina, syncope and congestive heart failure. The appearance of symptoms in patients with AS or ASAI gave a poor prognosis, with an average life span of approximately four years in medically treated patients. In contrast, a less lethal life history was noted in patients with AI, with variations depending on the etiology of the lesion. An understanding of the circulatory dynamics in patients with aortic valvular disease and the contrasts between volume overloading (AI) and pressure overloading (AS) is important in the use of the hemodynamic data in therapeutic interventions. Surgical therapy revealed a wide variation in operative mortality depending on the type of lesion. A significant correlation was noted between increasing numbers of clinical and hemodynamic parameters and operative mortality in patients with AS. No correlation was noted in patients with ASAI or AI, but operative mortality was significantly higher in patients with AI who had associated aortic root disease. The over-all long-term survival, state of clinical improvement and postsurgical complications varied with the different valvular lesions. The time at which surgical therapy appears appropriate and necessary is not uniform and varies with certain parameters described in the three types of aortic valve disease discussed.

In 60 patients with pure mitral stenosis, roentgenographic examinations of the chest were made within 30 days of complete right and left heart catheterization. The relative accuracy of the different roentgen signs in predicting a mitral valve area of 1.3 cm.2 or less was as follows: (1) Kerley's B lines—96 per cent; (2) combined venous and arterial abnormalities in the pulmonary vascular pattern—97 per cent; (3) left atrial enlargement producing more than 12 cm.2 posterior deviation of the esophagus—83 per cent; (4) either 1 or 2 plus 3—100 per cent. Marked left atrial enlargement correlated best with atrial fibrillation. For assessing pressures and the resistances, the abnormal pulmonary vascular pattern appeared to be more sensitive than Kerley's B lines. In predicting mean pulmonary arterial pressure, the pulmonary artery/hemithorax ratio was more accurate than the diameter of the right descending pulmonary artery.It is concluded that in addition to indicating specific hemodynamics, chest roentgenogram...

A patient with advanced rheumatoid arthritis, massive splenic enlargement and recurrent infections is described. Initially it was thought that the patient had a hematologic malignancy because of the unusually large size of the spleen. However, careful evaluation revealed hypersplenism of the neutropenic type. The patient underwent splenectomy with a favorable hematologic and clinical response. The size of the spleen proved to be the largest recorded in an uncomplicated case of Felty's syndrome. The literature is reviewed with emphasis on the variable features and the response to splenectomy in this syndrome.