Operator radiation exposure during percutaneous transluminal coronary angioplasty.

Operator radiation exposure during percutaneous transluminal coronary angioplasty as compared with that during routine coronary angiography is unknown. Therefore, cumulative radiation exposure at operator eye level was measured in two physicians (operators 1 and 2) during performance of coronary angioplasty and routine coronary angiography. The physicians participated together during angioplasty in eight patients; they performed routine angiography separately in eight patients each. Cumulative radiation exposure for eight angioplasty procedures was 140 mrads for operator 1 and 130 mrads for operator 2. In contrast, exposure during eight routine angiograms was 80 mrads for operator 1 and 60 mrads for operator 2. Mean cineangiographic time per case was similar (p = NS) during angioplasty (44.1 +/- 14.0 seconds for both operators) and angiography (49.7 +/- 6.1 seconds for operator 1, 47.6 +/- 16.1 seconds for operator 2). In contrast, fluoroscopy time was longer (p less than 0.01) for angioplasty (34.5 +/- 17.7 min) compared with angiography (13.1 +/- 5.1 min for operator 1, 13.7 +/- 8.2 min for operator 2). Thus, operator radiation exposure during percutaneous transluminal coronary angioplasty was, on average, 93% greater than during routine coronary angiography and was related to the duration of fluoroscopy rather than cineangiography.

Effects of morphine sulfate on human coronary blood flow.

Because morphine causes coronary vasoconstriction in conscious dogs, human coronary blood flow was measured with the thermodilution technique before and after administration of morphine sulfate, 0.2 mg/kg body weight (maximum 15 mg) intravenously, in 10 patients to determine if the canine experience is clinically applicable. Coronary blood flow increased from a baseline value of 104.4 +/- 13.4 (mean +/- standard error of the mean) to 113.0 +/- 17.4 ml/min (difference not significant) 15 minutes after the administration of morphine. Baseline coronary vascular resistance was 1.14 +/- 0.19 mm Hg/ml/min; 15 minutes after morphine administration the resistance value was 1.02 +/- 0.17 (P less than 0.025). There was no significant change between baseline values and values 15 minutes after morphine administration in systemic mean arterial pressure (98.2 +/- 5.3 to 92.8 +/- 4.7 mm Hg); heart rate (69.5 +/- 3.5 to 72.6 +/- 3.4 beats/min), left ventricular ejection time (0.345 +/- 0.009 to 0.342 +/- 0.007 second) or tension-time index (2,324 +/- 128 to 2,291 +/- 149 mm Hg/sec per min). The slight coronary vasodilation noted after morphine administration in this study is in marked contrast to the significant coronary vasoconstriction demonstrated in the unanesthetized dog.

Propranolol rebound--a retrospective study.

To assess the effects of sudden withdrawal of propranolol on inpatients with coronary artery disease, 102 patients admitted for cardiac catheterization were evaluated. Criteria for inclusion in the study were angiographically documented coronary artery disease, propranolol therapy at a mean daily dose of at least 80 mg and abrupt discontinuation of propranolol therapy before catheterization. There were 55 patients (mean age 52.5) who discontinued propranolol therapy (mean daily dose 127 mg) and a control group of 47 patients (mean age 53) who continued to receive propranolol (mean daily dose 143 mg). The criteria for morbidity were death, myocardial infarction or change in pain pattern. In the withdrawal group there were no deaths, one myocardial infarction judged to be related to catheterization and only one instance of a change in pain pattern. Thus, propranolol rebound appears to occur infrequently among hospitalized patients with reduced activity.

Coronary artery bypass surgery; a stimulus to modify existing risk factors?

Coronary arterial atherosclerosis is known to be associated with the risk factors of a positive family history, smoking, systemic hypertension, diabetes mellitus, and elevated serum cholesterol levels. Modification of these risk factors, where possible, is prudent. The risk factor data of 226 (212 men, 14 women) subjects who underwent coronary artery bypass surgery for symptomatic obstructive coronary artery disease are presented. Prior to surgery, an attempt was made to educate the subjects in regard to the risk factors and they were urged to modify these factors. All underwent repeat evaluation one year after operation. Although over half of the subjects had had a prior myocardial infarction and all had had aortocoronary bypass surgery, strong stimuli to modify risk factors, there was little modification of the risk factors of smoking and serum cholesterol. There was some modification of the hypertension risk factor. This study documents the need for a very early approach in life to prevent acquiring risk factors and the need for more research into better methods of behavior modification in the adult population.

Persistence of biologic activity after disappearance of propranolol from the serum.

In order to evaluate the duration of the biologic effects of propranolol after the drug was discontinued, we evaluated a variety of noninvasively determined hemodynamic parameters. Significant depression was found in the heart rate (18 per cent), cardiac output (13 per cent) (determined echocardiographically), and the triple product of blood pressure, heart rate, and systolic ejection time (16 per per cent) during administration or propranolol (200 mg. per day) to 9 normal volunteers. Significant depression of these parameters was present 12 hours after discontinuing the drug. By 12 hours, serum propranolol levels had returned 90 per cent toward their base line; however, at the same time, the heart rate and cardiac output had returned only 19.4 and 14.3 per cent toward their base-line values, and the triple product had returned 41 per cent toward its baseline. By 36 hours no biologic effect was seen. Thus if propranolol were discontinued 2 days prior to cardiac surgery, no significant biologic effect would remain to complicate the patient's postoperative course.

Diagnosis and management of myocardial ischemia in the postoperative period.

The determinants of myocardial oxygen consumption, the consequences of coronary artery atherosclerosis, angina, and myocardial infarction, and their therapy are considered in this article. The mechanism of action of the drugs used in the therapy of myocardial ischemia and the rationale for their use is discussed. A plan of in-hospital rehabilitation for the postoperative myocardial infarction patient is also offered.

Management of acute chest pain syndrome.

In differentiating the various etiologies of acute chest pain syndromes, the clinician is faced with identifying life-threatening situations. This article has presented a diagnostic approach for establishing the cardiovascular and noncardiovascular etiologies of acute chest pain syndromes. Cardiovascular etiologies must be identified early upon presentation in order to minimize morbidity and mortality. Myocardial ischemia and particularly necrosis is time dependent: early intervention preserves myocardium, particularly when initiating thrombolytic therapy. Aortic valvular disease, particularly critical aortic stenosis, if unrecognized, can precipitate rapid patient deterioration if inappropriately treated with nitrate therapy for presumed ischemic disease. Aortic dissection, if not properly diagnosed, can progress to stroke, MI, paralysis, and death. Noncardiovascular etiologies are similarly complex but often have less potential for life-threatening consequences. In identifying gastrointestinal bleeding, a careful rectal exam may be safely performed even in the setting of MI. A tension pneumothorax can suddenly compromise vascular return and progress to sudden death if unrecognized. Finally, chest wall symptoms, though seldom life-threatening, can be debilitating to the patient and often respond to anti-inflammatory therapy. In conclusion, the goals of this article were to present a step-wise approach to the diagnosis and management of an often complex presentation. By systematically approaching these patients with a thorough understanding of etiologies, diagnostic options, and therapeutic considerations, both physician anxiety as well as patient complications will be greatly diminished.

Angina pectoris. Diagnosis and treatment.

The physician who understands the pathophysiology of angina pectoris can apply rational therapeutic measures based on an appreciation of the determinants of myocardial oxygen supply and demand. Most patients with angina secondary to coronary atherosclerosis can be treated conservatively using a systematic approach that includes correction or removal of underlying causes or precipitating factors and the judicious use of sublingual nitroglycerin. In patients with more resistant angina, use of oral or topical nitroglycerin or sublingual isosorbide dinitrite as well as propranolol can be advised. Aortocoronary bypass surgery can offer significant improvement in carefully selected patients with frequent angina poorly controlled by medical therapy. The most important consideration in the treatment of angina is protection of coronary blood flow reserve by primary prevention of the atherosclerotic process itself. All individuals from families prone to coronary artery disease should be evaluated for alterable risk factors, the most important being cigarette smoking, hypertension, and hypercholesterolemia. Considering the high risk of unheralded sudden death in previously asymptomatic patients with coronary atherosclerosis, angina can, in a sense, be considered a fortunate harbinger of coronary stenosis, identifying candidates for secondary preventive measures aimed at retarding the progression of vascular disease. More importantly, angina serves as an index for detecting families at high risk of coronary artery disease, in whom early application of primary prevention may afford a more promising outlook.

What is the appropriate "dress code" for the cardiac catheterization laboratory?

In order to determine the effect of the manner of dress by personnel and observers on cardiac catheterization-related infections, a retrospective survey was undertaken of 107,203 catheterization procedures done during the calendar year prior to this survey. An analysis of 55,976 cutdowns and 53,578 percutaneous procedures was performed (some subjects had both procedures performed). A total of 379 infections in 109,554 entrance sites were reported for an overall incidence of infection of 0.35%. There were 33 infections at the percutaneous site (incidence = 0.06%) and 346 at the cutdown site (incidence = 0.62%). The manner of dress of personnel not involved with catheter manipulation and of the observers had no relationship to the incidence of infection when the percutaneous technique was used. When cutdowns were performed, there was a lower incidence of infection in those laboratories where all personnel and observers were required to wear a mask, cap, and gown (17,311 cutdowns, 83 infections, 0.48% infection rate) than in those laboratories where none of these was required (15,170 cutdowns, 109 infections, 0.72% infection rate) (P less than 0.025). Laboratories which did 150 or less cutdowns/year had more infections than those laboratories performing more than 150/year (P less than 0.0001). Our data suggest that the risk of infection from cardiac catheterization is more closely correlated with the volume of studies done in the laboratory than in the manner of dress of the laboratory personnel and visitors in the laboratory. However, the wearing of full "sanitary clothing" will help decrease the infection rate in cutdowns.

Effect of morphine on splanchnic blood flow.

Splanchnic blood flow was measured by the constant infusion of indocyanine green given before and after morphine 0.2 mg/kg (maximum 15 mg) intravenously in 13 patients. Splanchnic blood flow increased from 1012 +/- 98 ml/min to 1200 +/- 118 ml/min after the administration of morphine, a 19 per cent increase (P less than 0.025). Splanchnic vascular resistance decreased from 0.094 +/- 0.010 to 0.081 +/- 0.010 mmHg min/ml, a 16 per cent decrease (P less than 0.001). There was no significant change between baseline and post-morphine values in systemic arterial pressure (92.2 +/- 3.8 and 89.0 +/- 2.9 mmHg), hepatic vein wedge pressure (7.1 +/- 1.0 and 7.8 +/- 0.6 mmHg), or right atrial mean pressure (4.5 +/- 0.6 and 4.3 +/- 0.7 mmHg). This study shows that morphine induced significant splanchnic arteriolar dilatation.

The effects of morphine on venous tone in patients with acute pulmonary edema.

In order to compare the venodilation effect of morphine in normal individuals (22) with that in patients (13) with heart failure morphine sulfate (0.1 mg/kg) was administered to 13 patients with mild pulmonary edema. After morphine congestive symptoms improved and venodilation was induced as determined by two independent techniques: venous pressure fell 10.2 mm Hg by the isolated hand technique and the venous volume of the forearm increased by 0.48 cc/100 ml, measured by equilibration technique. Neither finding differed from those in normal individuals. Reflex venoconstriction noted on the taking of a single deep breath was unaffected by morphine administration and was similar to that observed in normal subjects. Since the drug morphine sulfate does not cause a major pooling of blood in the limbs, the favorable effect of narcotics in patients with pulmonary edema must be caused by other mechanisms such as splanchnic pooling, afterload reduction or reduced breathing effort.

Recurrent pulmonary emboli secondary to right atrial thrombus around a permanent pacing catheter: a case report and review of the literature.

This report describes the management of a woman with multiple pulmonary emboli secondary to a large right atrial clot which had formed around her permanent transvenous pacemaker. She continued to have pulmonary emboli despite adequate anticoagulation. Removal of the catheter and pacing required right atriotomy under cover of cardiopulmonary bypass. Additionally, eight English language case reports of symptomatic pericatheter thromboses are reviewed. In these cases, pericatheter clot resulted either in right-sided inlet obstruction or pulmonary emboli. The mortality rate was 75%. Although the cause for our patent's thromboembolic events is uncertain, congestive heart failure was a predisposing factor in 75% of the other reported cases. We suggest that pacemaker patients in congestive heart failure might benefit greatly from chronic anticoagulation.

Diffuse coronary artery disease in diabetic patients: fact or fiction?

To compare angiographically-determined coronary artery disease in diabetic patients with controls, 1,653 patients coming to cardiac catheterization were reviewed retrospectively to find 37 diabetic and 79 control patients matched for sex, age (+/- 3 years), and risk factors (hypertension, hyperlipidemia, and smoking). The severity of coronary artery disease was assessed using an angiographic grading system. The following results were obtained: 16 of 37 diabetic patients (43%) had three-vessel disease compared to 20 of 79 controls (25%). Seventy-six of 111 (68%) diabetic vessels were diseased compared to 110 of 237 control vessels (46%) (P less than 0.005). The total coronary score reflecting total extent of disease for diabetic patients was 371 (mean 10.0 +/- (SEM) compared to 594 for controls (mean 7.5 +/- 0.7, (P less than 0.01). Diabetic patients had a statistically similar number of diffusely diseased vessels as controls (28% vs 22%). There were only three of 76 diabetic vessels (4%) considered inoperable compared to seven of 110 (6%) control vessels. We conclude that diabetic patients with chest pain have more coronary artery disease than nondiabetics, but no more diffuse or inoperable disease.

Detection of tricuspid regurgitation and estimation of central venous pressure by two-dimensional contrast echocardiography of the right superior hepatic vein.

Two-dimensional echocardiography (2DE) was utilized to visualize the right superior hepatic vein (RSHV) for detection of tricuspid regurgitation (TR) and estimation of central venous pressure (CVP). Patients were divided into two groups. Eighteen patients were placed in group I on the basis of typical clinical features of TR (five patients) or 2DE contrast evidence of TR (13 patients). Group II included 55 patients without TR. Maximal transverse dimension of RSHV of at least 1.8 cm (range 1.8 to 3.8 cm, mean 2.4 cm) identified all patients in group I (100% sensitivity). One patient in Group II had RSHV width of 2.1 cm (96% specificity). Predictive value was 95%. RSHV width ranged from 0.4 to 2.1 cm (mean 1.3 cm) in group II. Mean values for group I and II were significantly different (p less than 0.001). Linear regression analysis was utilized to compare CVP and maximal RSHV width in 42 patients (15 group I and 27 group II). The slope of the line was significantly different from zero (p less than 0.005); the correlation coefficient was 0.70. In patients with maximal RSHV width greater than 1.5 cm, the predictive value for elevated CVP (greater than 6 mm Hg) was 87% with 69% sensitivity and 78% specificity. In 13 group II patients with technically satisfactory 2DE but no distinctly visible RSHV, CVP ranged from 4 to 12 mm Hg with four elevated values (greater than 6 mm Hg). Predictive value of normal CVP in absence of visible RSHV was 69%. This study suggests that determination of maximal RSHV width is useful in detection of TR and may be helpful in estimation of CVP.