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Fifty-seven patients undergoing various cardiac operations were managed with delayed sternal closure because of ongoing mediastinal hemorrhage or extreme cardiac dilatation. This strategy facilitated rapid access to the mediastinum for evacuation of clot when the risk of tamponade from hemorrhage was deemed great. When sternal closure over a dilated and edematous heart caused hemodynamically significant cardiac compression, wound closure without sternal reapproximation facilitated hemodynamic stability. Postoperative correction of hemodynamic and hemostatic functions allowed delayed sternal closure to be done a mean of 2.8 days later. Thirty-eight patients survived to leave the hospital. Recognized complications of delayed sternal closure included superficial wound infection (3 patients), sternal osteomyelitis (1 patient), and fatal mediastinal infection (1 patient). Delayed sternal closure may be beneficial in selected patients. Morbidity and mortality related to this technique have proved acceptable in this high-risk group.

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The external carotid artery (ECA) is an underestimated but important collateral to the cerebral hemisphere and eye in patients with severe disease of the internal carotid artery. Fifteen symptomatic patients with total occlusion of the internal carotid artery underwent ECA reconstruction. Ipsilateral ECA reconstruction was performed upon all patients with no mortality or neurologic deficits. Contralateral disease of the carotid artery was noted in 11 and required correction in seven patients. Follow-up study of the patients ranged from one to 68 months (a mean of 26.8 months) after operation. Vertebrobasilar symptoms persisted in two patients, both with contralateral disease. One of these patients successfully underwent extracranial-intracranial bypass. One ipsilateral and one contralateral stroke occurred during follow-up study, both in patients with contralateral disease. Eleven patients were alive and asymptomatic at last follow-up examination. Symptomatic selected patients with occlusion of the internal carotid artery and ECA stenosis or cul-de-sac formation should be considered for operation. ECA reconstruction is associated with little morbidity and three-fourths of the patients remain asymptomatic. A high incidence of contralateral disease of the carotid artery is present. Extracranial-intracranial bypass should only be considered when symptoms persist after correction of contralateral disease of the carotid artery and any ECA lesions.

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The treatment of accidental hypothermia by extracorporeal circulation and internal rewarming can be life saving in patients unconscious from drug overdose or victims of accidental exposure to severe cold. Advantages are the rapidity of treatment, the provision of circulatory support, and a lessened chance of rewarming collapse, since peripheral vasodilation is paralleled by an increase in cardiac output. A premature diagnosis of clinical death was averted in two patients with rectal temperatures of 25 degrees C or below, and their lives were saved by the use of this technique.

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An air gun pellet cardiac injury, in which there was penetration through the right ventricle, interventricular septum, and anterior papillary muscle and ejection from the left ventricle, is described. The pellet embolus was removed from the left popliteal artery with restoration of flow. The particular implications of pellet embolization are discussed and contrasted with those of bullet embolism.

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The natural history of totally occluded internal and common carotid arteries was studied in 102 patients (109 arteries) with a 97 percent follow-up (mean 39.7 months.) Symptomatic occlusions occurred in 72.6 percent of the patients, the reconstructed group (46 patients) having a greater number of symptomatic vessels than the nonreconstructed group (63 patients) (p less than 0.05). Contralateral disease was encountered in 46 percent. Initial mortality was 5 percent. Twenty patients (19.6 percent) were dead at the time of follow-up. Half of these deaths were from strokes and three fourths from atherosclerotic causes. Persisting neurologic symptoms were present in 14 percent of the patients and new events occurred in 5 percent. Fifteen percent of initially asymptomatic vessels were symptomatic at last follow-up. Twenty-one percent of the symptomatic occluded vessels were symptomatic on follow-up, 16 percent being in the reconstructed group and 26 percent in the nonreconstructed group.

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The adenine nucleotide content of the human myocardium in the distribution of the left anterior descending coronary artery (LAD) was measured before and after saphenous vein bypass grafting. The purpose of the study were twofold: (1) to relate the level of adenosine triphosphate (ATP) before bypass grafting to the percent stenoses of the LAD and (2) to determine the benefit or lack of benefit of bypass grafting on ATP content. Eighteen patients with angiographically determined LAD lesions of 40% to 100% underwent bypass grafting with standard cardiopulmonary bypass and cardioplegia. Transmural needle biopsy specimens were obtained from the center of the area perfused by the LAD immediately before cross-clamping of the aorta and 30 minutes after reperfusion of the myocardium via the native LAD and the graft. The tissue was divided into thirds: The endocardial and epicardial thirds were analyzed for ATP by high-pressure liquid chromatography and the middle third was viewed by light microscopy. The percent narrowing of the LAD correlated well (r = -0.71) with the ratio of ATP to total adenine nucleotides (TAN) in the endocardium. Epicardial ATP did not correlate with the percent stenoses of the LAD. The endocardial ATP/TAN ratio increased in the group as a whole from 0.51 +/- 0.27 (mean +/- SD) to 0.64 +/- 0.26 (p less than 0.01) after bypass grafting, and this was most impressive in those eight patients with LAD lesions greater than 90% (0.32 +/- 0.20 before grafting to 0.60 +/- 0.29 after grafting, p less than 0.005). However, the epicardial ATP/TAN ratio decreased from 0.75 +/- 0.15 before grafting to 0.64 +/- 0.17 after grafting (p less than 0.05), and this decrease occurred regardless of the percent narrowing of the LAD. There was no difference in vacuolization between the pre-grafting and post-grafting biopsy specimens, and intramyocardial hemorrhage was not observed. This study has demonstrated a close relationship between the degree of LAD stenosis and endocardial ATP content. Also, the endocardium supplied by arteries with greater than 90% lesions had significantly increased ATP while the epicardium had decreased ATP content after bypass grafting.

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This study correlates left atrial appendage cell size, atrial fibrosis and echocardiographic (echo) measurement of left atrial size with P wave morphology. Twelve patients with known mitral valve disease had echo measurements of left atrial size with P wave morphology. Twelve patients with known mitral valve disease had echo measurements of left atrial size prior to mitral valve surgery; patients had varying degrees of left atrial enlargement. The left atrial appendage, removed at the time of surgery, was stereologically assessed for percent fibrosis and the diameters of 50 cells were measured and averaged. These factors were correlated with P wave amplitude and duration in lead II, greatest length in any led, PR segment (end of P wave to onset of QRS), P to PR segment ratio (in lead II) and the PR interval. There was a good correlation of left atrial cell diameter with P wave amplitude (r = .69, p = 0.01). There was a good inverse correlation of percent fibrosis with the PR segment (r = -.72, p = 0.01) and a direct correlation of fibrosis with the ratio of P wave length to PR segment (r = .67 p = 0.01). There was a trend for percent fibrosis to correlate with PO wave duration but not height. No correlation was noted for any of the P wave characteristics and left atrial size. This study demonstrates that there is a correlation of P wave height with cell diameter and P wave length and PR segment with fibrosis. These data are helpful in understanding the electrocardiographic P wave.

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This report describes a patient who survived rupture of the left ventricular free wall following a myocardial infarction and who then subsequently went on to develop a pseudoaneurysm. The rupture became clinically recognized when the patient developed cardiac tamponade. A large hemopericardium was evacuated by performing a thoracotomy and a pericardiotomy. Although not evident at the time of the initial catheterization, a pseudoaneurysm developed over the ensuing months. The aneurysm was initially recognized by radionuclide angiography and confirmed by left ventricular angiography at a second cardiac catheterization. The aneurysm was successfully resected, and the patient was alive and functioning normally 18 months after rupture and 12 months after aneurysmectomy.

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Afterload reduction has become a routine treatment of patients with severe heart failure. In order to investigate the effect of afterload changes on indices of left ventricular performance, seven anesthetized dogs were studied. Serial alterations of afterload were produced with sodium nitroprusside and methoxamine infusions while the heart rate was maintained constant with right atrial pacing (120/min). High fidelity left ventricular (LV) pressure, aortic pressure (AoP) and systolic time intervals (STI) were measured simultaneously as a control and each time with the AoP changes. LV max dp/dt was measured by an RC differentiation and DP/DT was calculated from the pressure pulses and systolic time intervals. Each change in AoP resulted in a significant change in isovolumic pressure (IP) and the changes were parallel. Changes in pre-ejection period (PEP) and LV max (dp/dt)/(IP) were parallel changes in IP. A significant direct relationship was found between changes in IP and PEP, and an inverse relationship existed between changes in PEP and LV max (dp/dt)/(IP). Changes in LV max dp/dt and calculated DP/DT were parallel and approached unity. Thus, afterload changes with resultant changes in IP directly alter PEP and inversely affect max (dp/dt)/(IP). These effects of pure afterload changes must be considered in clinical pharmacologic studies when LV contractility is evaluated. Furthermore, calculated DP/DT can be used to measure changes in max dp/dt because of the close relationship between these two parameters.

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A quantitative study of the en face size and shape of rabbit endothelial cells from the ventral mid-thoracic and ventral infrarenal abdominal aorta has been carried out in 6 rabbits. Photomicrographs were taken from vascular casts of the rabbit aorta and the endothelial cell outlines were analyzed quantitatively using a digitizer and digital computer. The morphology of the endothelial cells was described using 8 calculated parameters (area, perimeter, length, width, angle of orientation, width:length ratio, axis intersection ratio and shape index). The endothelial cells in both locations had the same surface area (P greater than 0.30); however, the cells in the abdominal aorta were longer (P less than 0.01) and narrower (P less than 0.01) than those in the thoracic aorta. This fact is reflected by the smaller value for the shape index and width : length ratio in the abdominal aorta (P less than 0.01). Cells in both the thoracic and abdominal aorta were aligned with the flow direction.

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The factors contributing to early thrombosis or late intimal proliferation in arterialized vein grafts were studied in seven dogs. Autologous jugular veins replaced a segment of the cervical carotid artery bilaterally. Thirty minutes after graft installation and six months later, graft and proximal artery diameter, arterial pressure and blood flow were measured and wall tension, vascular resistance, flow velocity and energy loss between proximal artery and graft were computed. The diameter ratio of proximal artery to graft increased by 37% (p less than 0.05). Velocity of flow within the graft averaged 87% less than that in the proximal artery (p less than 0.05) and decreased by 58% after six months (p less than 0.05). Graft wall tension at both experimental periods was significantly higher than that of the proximal artery (p less than 0.05), increasing over six months by 91% (p less than 0.05). These results support contentions that low flow velocity contributes to early thrombosis of the graft and, that increased wall tension is significant factor in the pathogenesis of intimal thickening.

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A case of pacemaker malfunction in a permanently implanted demand transvenous pacemaker is presented. Complete "failure to sense," resulting in considerable hemodynamic embarrassment, was treated by chest wall stimulation using an external pacemaker and two superficial chest leads applied over the permanent pacemaker generator-lead junction. The technique of this procedure and its usefulness in the localization and temporary therapy of pacemaker sensing failure are discussed.

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A patient presented with mitral valve prolapse, ruptured chordae tendineae, severe mitral regurgitation and congestive heart failure. Pathologic studies demonstrated myxomatous changes of both mitral leaflets. Collagen analysis of the valve and of the chordae tendineae revealed the presence of type I collagen in normal quantities and a striking absence of type III and AB collagens. The altered collagen in this patient's mitral valve probably contributed to the development of his mitral valve disorder.

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Diastolic time (DT) calculated as the cycle length minus electromechanical systole (QS2) has a nonlinear relationship to heart rate (HR), increasing rapidly as rates fall below 75. The effect of propranolol on DT was studied in 150 patients with coronary artery disease. Patients were divided into three groups. Group I included patients with stable angina pectoris: propranolol (2.5 mg, i.v.) significantly increased DT from 411 +/- 18 to 527 +/- 22 msec (p less than 0.001) in 23 patients of group I; therapy with propranolol (mean daily dose 200 +/- 15 mg) increased DT from 446 +/- 29 to 766 +/- 26 msec (p less than 0.001) in 15 patients with stable angina. Group II was made up of patients with acute myocardial infarction: Propranolol (2.5 mg, i.v.) increased DT from 379 +/- 16 to 458 +/- 24 (p less than 0.001) in 18 of these patients. Group III included patients with recent coronary bypass surgery: propranolol (2.5 mg, i.v.) increased DT from 323 +/- 9 to 468 +/- 24 msec (p less than 0.001) in 14 patients 7 days after surgery. In addition, DT at 15 hr and 2 weeks after surgery was compared in 30 patients maintained on propranolol (mean daily dose, 155 +/- 11 mg preoperative and 68 +/- 9 mg postoperative) and 50 other patients who underwent coronary bypass surgery not on propranolol. DT was greater in propranolol patients (546 +/- 21 vs. 388 +/- 16 msec, p less than 0.001), preoperative and 396 +/- 15 vs. 320 +/- 12 msec, p less than 0.001, postoperative). Changes in DT after propranolol are mainly attributed to decreased HR. Changes in QS2 were much less profound and always less (p less than 0.01) than changes in DT. Thus propranolol significantly increased DT per beat in patients with coronary artery disease, which allowed more time for coronary perfusion; this effect of propranolol could well be as important as the reduction of myocardial oxygen consumption.

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Seventy-nine patients undergoing staged bilateral carotid endarterectomy were studied to determine the relationship of perioperative hypertension to postoperative neurologic deficits. Six of the eight neurologic deficits following 158 endarterectomies (5%) occurred after the first operation, all being temporary. Comparison of the mean blood pressures in patients with and without postoperative strokes revealed no statistically significant differences. Patients on antihypertensive medications were at a significantly higher risk of developing postoperative strokes. A trend towards higher blood pressure was noted following the second endarterectomy, particularly when they were staged more than 60 days apart. Based on our findings, a cautious approach is warranted in the treatment of postendarterectomy hypertension.

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The safety and beneficial effect of continuation of propranolol (Pr) through coronary bypass surgery (CBS) was studied in two groups of patients. In the control group (50 patients) Pr was discontinued 24 h before CBS without reinstitution afterwards. In the propranolol group the drug was maintained up to 4 to 10 h before surgery and was restarted within 24 h afterwards. The incidence of subendocardial myocardial infarction was significantly lower in the Pr group (1 out of 30 vs 10 out of 50, p less than 0.05) while the incidence of transmural infarction was the same in both groups (3 out of 30, 10%, vs 5 out of 50, 10%). The incidence of supraventricular tachycardias during the first three postoperative days was significantly lower in the propranolol group compared to control (5% vs 30%, p less than 0.01). The 24 h urinary epinephrine and norepinephrine excretion was significantly greater than normal the day before surgery (136 +/- 12 vs 39 +/- 4 micrograms/24 h, p less than 0.01), and was still high two weeks after surgery (115.1 +/- 14 micrograms/24 h). There were no complications related to propranolol. The left ventricular function as measured from the systolic time intervals was the same pre- and postoperatively in both groups. The results of this study show that administration of propranolol up to 4 h before coronary bypass and reinstitution immediately afterwards is safe and beneficial.

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