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R W DeSanctis

Publications and source records attributed to R W DeSanctis.

At least 19 recordsLinked to original sources

Aortic dissection.

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Aortic Dissection

Stroke following coronary-artery bypass surgery. A case-control estimate of the risk from carotid bruits.

The causes of stroke following coronary-artery bypass surgery are largely unknown. To determine whether carotid bruits increase the risk of these events, we compared 54 patients with postoperative stroke or transient ischemic attacks with 54 randomly selected control patients. Both groups were drawn from 5915 consecutive patients who had coronary bypass surgery at our hospital from 1970 to 1984. Carotid bruits were noted preoperatively in 13 patients with postoperative stroke and in 4 control patients. Case-control analysis showed that the presence of carotid bruits increased the risk of stroke or transient ischemic attacks by 3.9-fold (95 percent confidence interval, 1.2 to 12.8; P less than 0.05). This increased risk remained essentially unchanged after adjustment for potentially confounding variables in a multiple logistic regression analysis. Other factors associated with a significantly increased risk (P less than 0.05) of these neurologic deficits were a history of stroke or transient ischemic attack (odds ratio, 6.0; 95 percent confidence interval, 1.6 to 22.1), a history of congestive heart failure (odds ratio, 5.3; confidence interval, 1.6 to 17.0), mitral regurgitation (odds ratio, 4.3; confidence interval, 1.4 to 12.9), postoperative atrial fibrillation (odds ratio, 3.0; confidence interval, 1.4 to 6.7), a cardiopulmonary-bypass pump time of more than two hours (odds ratio, 2.7; confidence interval, 1.1 to 6.7), and a previous myocardial infarction (odds ratio, 2.3; confidence interval, 1.1 to 5.1). We conclude that the presence of carotid bruits increases the risk of stroke after coronary-artery bypass surgery. However, the absolute magnitude of this risk, 2.9 percent, is small and comparable to the reported risk of stroke from carotid endarterectomy.

Atrial Fibrillation

Aortic dissection.

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Aortic Dissection

Spectrum of conditions initially suggesting acute aortic dissection but with negative aortograms.

Between 1963 and 1983, 55 patients presented to our hospital with a clinical picture that suggested aortic dissection but with aortograms that were interpreted as negative for that entity. In 4 patients, the aortographic findings subsequently proved to be false negative. The remaining 51 patients had the following diagnoses: myocardial infarction in 9 patients; aortic regurgitation in 5; thoracic nondissecting aneurysm in 4; musculoskeletal pain in 4; mediastinal tumor in 4; pericarditis in 3; acute coronary insufficiency in 3; cholecystitis in 2; miscellaneous in 3; and unknown in 14. The clinical features in these patients were compared with those of 125 patients with true aortic dissection. Three features were significantly more prevalent in patients with than without dissection: prior systemic hypertension, pain for 24 hours or less, and migratory pain. Patients without dissection were younger than those with distal dissection and had significantly less systemic hypertension, posterior thoracic pain and migratory pain. Patients without dissection had significantly less frequent congestive heart failure, pulse deficits and aortic regurgitation, and more frequent hypertension and pain for more than 24 hours than patients with proximal dissection. This study defines the actual differential diagnosis of aortic dissection at our hospital, the frequency of false-negative aortographic findings and contrasts the clinical features of patients with and without dissection.

Age Factors

The incidence and pattern of angina prior to acute myocardial infarction: a study of 577 cases.

In order to determine the incidence and pattern of angina as a premonitory symptom of acute myocardial infarction, 577 consecutive patients with acute myocardial infarction were questioned shortly after hospital admission about the presence and pattern of chest pain prior to onset of infarction, with particular emphasis on the month prior to infarction. Two hundred and seventy-six patients (48 per cent) had no angina before infarction (Group I), whereas 301 (52 per cent) did. One hundred and seventy-nine patients (31 per cent) had a history of chronic angina, and of these, 75 had no change in the pattern of angina prior to infarction (Group II) while 104 noticed worsening of their symptoms in the month prior to infarction (Group III). One hundred and twenty-two patients (21 per cent) had new onset angina in the month prior to infarction (Group IV). The number of patients with unstable angina prior to infarction (Groups III and IV) was therefore 226 or 39 per cent of the total series. In patients with unstable angina, the increase in severity of symptoms or the development of new onset angina occurred within a period of 1 week or less in 69 per cent. Patients with a history of previous infarction or chronic angina had a higher incidence of unstable angina prior to infarction than patients without such a history (p less than 0.05). Patients with prior angina (Groups II, III, and IV) had a higher incidence of subendocardial infarction than patients without angina (p less than 0.05). The hospital mortality rate in the four groups did not differ significantly.

Age Factors

Dissection of the aorta.

Our approach to management, both initial and definitive, is summarized in Table 2. Patients with proximal dissection require surgical intervention after medical stabilization, unless prior debilitating illness precludes general anesthesia or prolonged vascular surgery. If myocardial infarction or cerebrovascular accidents has complicated the dissection, results are extremely poor, regardless of therapy. Patients with distal dissection have a good prognosis with medical therapy alone, unless aortic rupture or impending rupture, hematoma progression despite a maximal drug program, vital organ compromise, or inability to control pain or blood pressure medically supervene. Dissecting aneurysm of the aorta, while potentially a promptly fatal event, is amenable to aggressive therapy provided that one is alert to the possibility of this disease. Despite all technical advances, the single most important factor in making the diagnosis of dissecting aortic aneurysm is a strong index of suspicion on the part of the physician.

Aged

Variant angina. Clinical spectrum and results of medical and surgical therapy.

Fifty-four patients with variant angina are described. They are divided into patients without hemodynamically (less than 50%) important coronary artery lesions (Group 1), patients with intermediate (greater than or equal to 50% and less than 90%) fixed obstruction (Group 2A), and patients with high grade (greater than or equal to 90%) fixed obstruction (Group 2B). Inferior ischemia occurred significantly more often in Group 1 (90% versus 33%. p less than 0.001), and exertional angina was more frequent in Group 2 (70% versus 36%, p less than 0.05). Maximum medical therapy with propranolol and nitrates failed to control angina in 55% of Group 1, 69% of Group 2A, and 63% of Group 2B. Twelve patients underwent intra-aortic balloon pumping (IABP), and in 10 there was complete control of variant angina. A total of 35 Group I patients underwent coronary artery bypass grafting (CABG), with a 2.9% mortality rate in patients without preoperative cardiogenic shock. Of these patients, 55% in Group 2A and 73% in Group 2B experienced marked improvement in their angina status. Therefore, we currently recommend bypass grafting for medically intractable variant angina in those patients with severely stenotic, fixed atherosclerotic lesions.

Angina Pectoris

Unexplained in-hospital fever following cardiac surgery. Natural history, relationship to postpericardiotomy syndrome, and a prospective study of therapy with indomethacin versus placebo.

In Part I of this study, the in-hospital course of 219 patients who had undergone a cardiac operation is analyzed. Fever (greater than or equal to 37.8 degrees C, rectal) was present after postoperative day 6 in 159 patients (73%) and was of unexplained cause in 118. Fever decay in the population of unexplained fever patients was exponential. All patients with unexplained postoperative fever were afebrile by postoperative day 19. In-hospital pericardial rub and pleuritic chest pain, widening of the mediastinum on chest film, and pleural effusion were not specifically associated with unexplained postoperative fever. In Part II, 67 patients with unexplained postoperative fever were given indomethacin (100 mg per day) or placebo for 7 days by a randomized, double-blind protocol. Indomethacin resulted in a shorter duration of fever (2.4 vs 3.5 days, P is less than 0.01) and in a shorter duration of chest pain, malaise, and myalgias compared to placebo. Sixty-seven percent of the patients in Part I and all of the patients in Part II were contacted 2-8 months following hospital discharge. Five percent had experienced an illness that we considered to be acute pericarditis, but its occurrence was unrelated to whether the patient had had in-hospital unexplained postoperative fever, in-hospital rub or chest pain, or in-hospital administration of indomethacin.

Cardiac Surgical Procedures

The clinical significance of bundle branch block complicating acute myocardial infarction. 1. Clinical characteristics, hospital mortality, and one-year follow-up.

To provide an understanding of the clinical characteristics of patients with acute myocardial infarction (MI) and bundle branch block, experience from five centers was accumulated. Patients in whom bundle branch block first appeared after the onset of cardiogenic shock were excluded. In 432 patients, the most common types of block were left (38%) and right with left anterior fascicular block (34%). In 42% of the patients, bundle branch block was new. Progression to high degree (second or third degree) atrioventricular (AV) block via a Type II pattern occurred in 22% of the patients. Hospital and first year follow-up mortality rates were 28% and 28%, respectively. Only 46% of the patients developed pulmonary edema or shock (Killip Class III or IV), and hospital mortality was related to the amount of heart failure (8%, 7%, 27%, 83% for Killip Classes I-IV, respectively). Patients with progression to second degree or third degree AV block via a Type II pattern had increased hospital mortality compared with patients without this complication (47% vs 23%, P less than 0.001). In the absence of pulmonary edema or shock, patients with Type II second degree or third degree AV block still had a higher mortality rate than patients without advanced AV block (31% vs 2%, P less than 0.005), with nearly all the deaths due to abrupt development of AV block. Thus, in many patients MI with bundle branch block is associated with severe heart failure. However, this was not true for a majority of the patients, in whom therapy aimed at preventing morbidity and mortality due to the bradyarrhythmia of advanced AV block might be beneficial.

Acute Disease

The clinical significance of bundle branch block complicating acute myocardial infarction. 2. Indications for temporary and permanent pacemaker insertion.

The indication for prophylactic temporary and permanent pacing during acute myocardial infarction (MI) complicated by bundle branch block is high risk of progression via a Type II pattern to second or third degree (high degree) AV block during hospitalization or follow-up. In this study, determinants of high degree AV block during hospitalization and sudden death or recurrent high degree block during the first year of follow-up were examined in 432 patients with MI and bundle branch block. Timing of onset of bundle branch block, the involved fascicles, and the PR interval were examined as determinants of risk of progression to high degree AV block during MI. At highest risk were 186 patients with blocks involving the right bundle and at least one fascicle of the left bundle which were not documented on prior electrocardiograms. Risk was similar with (38%) or without (31%) accompanying first degree AV block. Patients with transient high degree AV block during MI had a 28% incidence of sudden death or recurrent high degree block during the first year of follow-up. Patients not continuously paced had a higher incidence of sudden death or recurrent high degree block than patients continuously paced (65% vs 10%, P less than 0.001). Sudden death during follow-up also occurred in 13% of patients without high degree block during MI. A subgroup with 1) documented prior MI, 2) anterior or indeterminant acute MI, and 3) no symptoms of cardiac failure had a 35% risk of sudden death. The role of permanent pacing in this group is unknown. Thus, patients at high risk of high degree AV block should receive prophylactic temporary pacing. Patients who survive high degree block with MI should receive temporary and then permanent pacing. Patients without high degree AV block during MI who nervertheless have a high risk of sudden death may benefit from permanent pacing.

Adult

Aspirin prophylaxis of venous thromboembolism after total hip replacement.

We assessed aspirin prophylaxis against venous thromboembolism in a prospective, controlled, double-blind study of patients over 40 years of age, who had undergone total hip replacement. Radiographic phlebography was the diagnostic end point. Thromboembolism developed in 11 of 44 patients receiving aspirin, as compared to 23 of 51 receiving the placebo (P less than 0.03). Unexpectedly, this protection was limited to men. In four of 23 men on aspirin thrombi developed, as compared to 14 of 25 receiving placebo (P less than 0.01). Corresponding figures for women were seven of 21 versus nine of 26. Review of a similar group of patients receiving aspirin revealed significantly greater protection (P less than 0.03) in men (three of 15) than in women (15 of 27). These data establish statistically significant prophylaxis in men over the age of 40 by 600 mg of aspirin given twice daily. The absence of a protective effect in women remains unexplained.

Adult

The clinical recognition of dissecting aortic aneurysm.

The clinical, roentgenologic and laboratory findings in 124 patients with dissecting aneurysm of the aorta are reported. In 53 patients the dissection occurred in the ascending aorta ("proximal" dissection), and in 71 patients the site of origin was the descending thoracic aorta ("distal" dissection). Certain distinct clinical differences between the groups were apparent. Although hypertension was an important predisposing factor, it was significantly more common in distal dissection, as was atherosclerosis. Back pain and hypertension on hospital presentation characterized patients with distal dissection. Conversely patients with proximal dissection were younger and had a significantly higher incidence of Marfan's syndrome, cystic medial necrosis, anterior chest pain, pulse deficits, neurologic compromise, aortic insufficiency and congestive heart failure. In both groups, syncope appeared to correlate well with the occurrence of cardiac tamponade. Chest roentgenograms almost always showed an abnormal aortic contour. Aortic angiography, when performed, was usually confirmatory of the diagnosis.

Adult

Atrial tachyarrhythmias in acute myocardial infarction.

Causative factors, clinical consequences and treatment of atrial tachyarrhythmias were reviewed in 917 monitored patients with definite acute myocardial infarction. Significant atrial tachyarrhythmias were found in 104 (11 per cent) of them and included atrial fibrillation in 67, atrial flutter in 29 and paroxysmal atrial tachycardia in 33. These episodes were single in 79 patients and multiple in 25, and began within the first four days of acute myocardial infarction in 90 per cent of the patients. Fifty per cent of these atrial tachyarrhythmias were heralded by premature atrial contractions. The incidence of atrial tachyarrhythmia was not related to the location of the acute myocardial infarction or to the presence or degree of power failure; however, atrial tachyarrhythmias were significantly more frequent in patients with pericarditis. Atrial tachyarrhythmias were well tolerated in almost one fifth of the patients, caused marginal compromise in almost two thirds and led to severe clinical deterioration in one fifth. Paroxysmal atrial tachycardia rarely required specific treatment, atrial fibrillation was best managed with intravenous administration of digoxin except when associated with severe clinical compromise, and atrial flutter generally required cardioversion or rapid intravenous therapy and usually caused severe clinical deterioration. Over-all, atrial tachyarrhythmia was not associated with a significantly increased mortality, and in those who died, death was not related specifically to the atrial tachyarrhythmia but rather to the severity of the underlying acute myocardial infarction. However, persisting atrial tachyarrhythmias, particularly atrial flutter which tends to be refractory to both heart rate control and cardioversion, may contribute indirectly to morbidity and mortality.

Adult