Diana F. Guthaner

Altered Adrenergic Activity in Coronary Arterial Spasm: Insight Into Mechanism Based on Study of Coronary Hemodynamics and the Electrocardiogram

To elucidate the pathophysiologic mechanism of coronary arterial spasm, the hypothesis was examined that underlying alterations in sympathetic activity may account for this syndrome in some patients. Observations were directed to alterations in coronary arterial hemodynamics and the electrocardiogram. Spasm of the left anterior descending coronary artery produced a mean increase in coronary vascular resistance of 107 percent (P less than 0.05) in four patients in whom coronary sinus blood flow was measured with the thermodilution technique. The alpha adrenergic blocking agent phentolamine, given intravenously, acutely reversed coronary spasm and its clinical manifestations in eight patients and reduced coronary resistance. In four patients, administration of the long-acting oral alpha blocking agent phenoxybenzamine (20 to 80 mg/day) caused disappearance of symptoms during a follow-up period of 3 to 12 months. Transient prolongation of the corrected Q-T interval preceded spontaneous or ergonovine maleate-provoked coronary spasm in 11 patients with variant angina pectoris, whereas no significant change in the Q-T interval followed ergonovine administration in 27 control patients with atypical chest pain who did not have coronary spasm. T wave inversions in the resting electrocardiogram were normalized by isoproterenol infusion in one patient and by long-term phenoxybenzamine treatment in four patients with variant angina pectoris. These Q-T and T wave changes are analogous to those described with unilateral or asymmetric stellate ganglion stimulation in animals. These observations suggest that alterations in the sympathetic nervous system that are consistent with asymmetric stellate ganglion activity and transient alpha adrenergic receptor stimulation can presage the development of coronary arterial spasm in some patients with variant angina pectoris.

The effects of ergonovine maleate on coronary arterial size.

Changes in coronary arterial size due to ergonovine maleate are described and quantitated in 90 patients - 18 with typical angina pectoris, 56 with atypical chest pain, nine with variant angina pectoris, and seven heart transplant (allograft) recipients. We observed two angiographic changes in the diameter of coronary arteries: 1) spasm, which was characterized by occlusion or marked (>85%) focal or diffuse vessel narrowing, or 2) relatively mild and diffuse vessel narrowing, which was interpreted as the normal pharmacologic response to the drug. Serial bolus injections of 0.05 mg, 0.10 mg and 0.25 mg of ergonovine maleate produced diffuse narrowing of the diameter of coronary arteries of 10 ± 1.5%, 16 ± 1.4% and 20 ± 1.3% (mean ± SEM), respectively, in the 72 patients with anginal syndromes who did not develop coronary spasm. The degree of coronary arterial narrowing was the same in heart transplant recipients and in patients with normally innervated hearts who did not develop coronary spasm. We believe the normal pharmacologic response to ergonovine maleate was due to a direct vasoconstrictor action of the drug; this action was independent of neural control extrinsic to the heart.

Long-term serial angiographic studies after coronary artery bypass surgery.

Twenty-six patients underwent repeat coronary angiography 5-8 years after saphenous vein coronary artery bypass surgery (SVCABG). These patients were selected from the first cohort of 117 patients who had SVCABG because they had obtained essentially complete relief of angina, and because all grafts were patent at initial angiography 11.2 months (mean) after surgery. Of the 39 grafts (1.5 grafts per patient) patent at 1 year, 34 (87.2%) were patent at reexamination 76 months (mean) (range 65-103 months) after SVCABG. Graft occlusion could not be predicted by the early angiographic appearance of the graft itself or its proximal or distal anastomosis. In some cases, narrowing or irregularity consistent with intimal hyperplasia appeared to progress, while in others it developed at late follow-up. Progressive narrowing occurred in 96% (22 of 23 grafted vessels) of the native coronary arteries proximal to the graft anastomosis. Progression to a stenosis ⩽75% or total occlusion was seen distal to the graft anastomosis in eight of 39 grafts (20%). Of 103 nonbypassed major vessels, 56% showed some progression of disease and half of these progressed to significant stenoses (⩽75% luminal narrowing). There were no apparent predictors to indicate whether progression in nongrafted coronary arteries would occur preferentially in a previously stenotic or nonstenotic vessel, although 80% of vessels with initial stenoses ⩽75% progressed to total occlusion.

Fate of the False Lumen Following Surgical Repair of Aortic Dissections: An Angiographic Study

Postoperative angiography was performed in 27 patients who had surgical repair for aortic dissections. The ascending aorta was involved in 22 dissections (Type A), while in five dissections it was uninvolved (Type B). Findings were assessed between two weeks and 13 years postoperatively. Despite the primary surgical objective to abolish flow in the false lumen, the majority of patients, whether symptomatic or not, continued to harbor patent distal false channels. In certain cases, one or more vital aortic branches were perfused solely by the false lumen. Initial postoperative angiography is indicated for determined surgical results as well as the functional significance of late angiographic findings, should symptoms recur. Further extension of the initial dissection, redissection, or enlargement of localized saccular aneurysms may mandate late reoperation. These conditions manifest themselves by pain, aortic regurgitation, neurological sequelae, or compromise of blood flow to a vital organ or extremity.

The use of computed tomography in the diagnosis of coronary artery bypass graft patency.

In a preliminary evaluation of the use of dynamic computed tomography (CT) for the detection of patent aortocoronary bypass grafts, 30 patients were scanned either during the early postoperative peroid or after graft patency was determined by angiography. To visualize the proximal grafts, CT scans were taken through the aortic root following an intravenous bolus injection of contrast medium. Patent bypass grafts to the left anterior descending and right coronary arteries were demonstrated in 77.5%, while posterior grafts to the circumflex and obtuse marginal coronary arteries were detected in 40%. With its pontential for extracting dynamic events, CT scanning provides a new, noninvasive modality for the diagnosis of patent bypass grafts, which heretofore have only been visualized by selective angiography.

Organized left atrial mural thrombus demonstrated by coronary angiography

Small coronary artery fistulas terminating at the site of adherent, organized mural thrombi in the left atrial appendage were observed during selective coronary angiography in patients with mitral stenosis. The angiographic features of this abnormality can be distinguished from those of cardiac tumors, vascular malformations, and coronary artery fistulas that are not associated with organized thrombus. This coronary angiographic abnormality may indicate the presence of left atrial thrombus that is not revealed by echocardiography and is not manifest clinically by systemic emboli. The size of the collection of radiographic contrast material in the left atrium is not proportional to the size of the thrombus.

Combined azygous vein and subclavian artery injury in blunt chest trauma.

Blunt chest trauma resulting in azygous vein injury with associated mediastinal widening is described. Emergency operative intervention was required, and subsequent arteriography revealed initial transection of the subclavian artery requiring repair. The potential significance of mediastinal venous bleeding and the importance of arteriography in diagnosing occult arterial injury in this setting are emphasized.

Pulmonary artery surgical aneurysmorrhaphy: Where do we go from here?

Pulmonary artery aneurysm, in the absence of associated congenital heart disease, is an extremely rare entity; furthermore, only a modicum of therapeutic approaches for this entity has been described. The pathogenesis of this lesion is poorly understood, and indications for surgical intervention are difficult to derive due to the paucity of information which exists concerning the natural history of patients with pulmonary artery aneurysms. This dilemma is compounded by the uniformly anecdotal nature of previously published works. This editorial note illustrates the presentation and clinical course of a patient with an asymptomatic pulmonary artery aneurysm who was managed surgically, discusses the questions inherent in the decision to proceed with surgical intervention, and explores the current ignorance which surrounds such decisions; hopefully, this report will prompt renewed awareness of this entity and catalyze future efforts to elucidate more completely the natural history of patients with pulmonary artery aneurysms. Exemplary patient. A 66-year-old male was referred for evaluation of bilateral hilar masses. Progressive, marked radiologic enlargement of these masses over a ‘I-year period had been noted at another hospital (Fig. 1). A 100 pack-year history of cigarette abuse and a &year history of increasing dyspnea on exertion were noted. Pulmonary function testing revealed moderately severe chronic obstructive pulmonary disease. Two recent episodes of pneumonitis had been associated with hemoptysis. His past med-

Comparative recognition of left ventricular thrombi by echocardiography and cineangiography.

Studies performed in 47 patients, 11 of whom underwent surgery for aneurysmectomy and 36 of whom underwent cardiac transplantation, were reviewed to assess the diagnostic accuracies of cross sectional echocardiography and cineangiography in detecting left ventricular mural thrombi and the effect of anticoagulation treatment on the incidence of such thrombi. Cross sectional echocardiography in 37 patients and cineangiography in 26 (16 patients were examined by both methods) were analysed independently by sets of two observers experienced in the respective methods. All four observers were blinded to the pathological or surgical findings regarding mural thrombus. Mural thrombus was confirmed by pathological investigation in 14 of 47 (30%) cases; 11 of these 14 patients had intra-aneurysmal thrombi. The negative predictive value was quite good for both methods, but cross sectional echocardiography had a superior positive predictive value. This was due both to detailed soft tissue resolution by cross sectional echocardiography and to overdetection of mural thrombi by cineangiography in cases of aneurysms without mural thrombi. Mural thrombi were present in three of 20 patients with preceding anticoagulation and in 10 of 19 patients without anticoagulation. The results emphasise that cross sectional echocardiography is more reliable than cineangiography in recognising thrombi.

Coronary hemodynamic effects of ergonovine maleate in human subjects

The coronary hemodynamic effects of ergonovine maleate were examined in 15 patients with a chest pain syndrome not thought to be variant angina. Ergonovine was given intravenously in sequential doses of 0.05, 0.1 and 0.25 mg while measurements were made of systemic hemodynamic variables, coronary sinus blood flow and coronary arteriovenous oxygen difference at intervals during the protocol. Coronary arterial diameters were measured from the 35 mm cineangiogram. Despite an increase in myocardial metabolic demand, as estimated with the heart-rate-blood pressure product, there was no apparent increase in coronary vascular resistance. In addition, there was a significant widening of the coronary arteriovenous oxygen difference in five of the seven patients in whom it could be measured. However, neither chest pain nor ischemic electrocardiographic changes were evoked. Although ergonovine also produced a diminution in epicardial coronary arterial diameters, this effect was not sufficient to explain the absence of appropriate coronary vasodilation. These results suggest that ergonovine may limit the normal vasodilatory response of the arteriolar bed to increases in myocardial metabolic demand.