Surgical treatment of variant angina: use of plexectomy with aortocoronary bypass.

Bertrand, Michel E.; Lablanche, Jean M.; Rousseau, Michel F.; Warembourg, H; Stankowtak, C; Soots, G

doi:10.1161/01.cir.61.5.877

Cited by 63 publications

(29 citation statements)

References 15 publications

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“…• Cardiac denervation (plexectomy), sometimes with autotransplantation, has been attempted in some cases of refractory coronary spasm, but it has been definitively abandoned owing to the high rate of recurrence and complications [47].…”

Section: Refractory Coronary Artery Spasmmentioning

confidence: 99%

Coronary artery spasm

Lanza

Maseri

2000

Curr Treat Options Cardio Med

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Attacks of variant angina usually respond promptly to sublingual administration of short-acting nitrates (nitroglycerin, 0.3 to 0.4 mg, or isosorbide dinitrate, 5 to 10 mg), which may be repeated after 3 to 5 minutes if pain persists. In the rare cases resistant to sublingual nitrates, sublingual nifedipine (5 to 10 mg) or, when readily available, intravenous nitrates (nitroglycerin or isosorbide dinitrate, 2 to 10 mg) or calcium antagonists (verapamil, 5 to 10 mg, or diltiazem, 0.15 mg/kg) can be given. All attempts to prevent ischemic attacks by means of specific receptor blockade in patients with vasospastic angina have been unsatisfactory. This may be either because the doses of the blockers used were insufficient or, more likely, because the blockade of a single receptor-agonist interaction leaves receptors for other vasoconstrictor stimuli unopposed and therefore capable of eliciting spasm. Thus, for instance, alpha-adrenergic, serotoninergic, and thromboxane A(2) antagonists all failed to reduce significantly the number of anginal attacks, although they appeared to be effective in some patients. Until the actual causes of the coronary smooth muscle hyperreactivity to constrictor stimuli are known, treatment of vasospastic angina is based on the use of nonspecific vasodilators. Indeed, the mainstay of pharmacologic treatment of coronary artery spasm is calcium channel blocking agents together with nitrates to cover the periods in which spasm is most likely to occur. These powerful vasodilating agents, at their usual doses, are able immediately and completely to control the recurrences of ischemic attacks in as many as 80% of patients. Moreover, some studies have shown that use of calcium antagonists significantly improves clinical outcome in patients with variant angina.

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Section: Refractory Coronary Artery Spasmmentioning

confidence: 99%

Coronary artery spasm

Lanza

Maseri

2000

Curr Treat Options Cardio Med

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“…Variant angina can usually be controlled with calcium-antagonist drugs. 4 I Although patients with organic lesions often do well after bypass surgery,6 7 the results are poorer than in other subsets of coronary disease,8 9 and variant angina may occur after surgery in spite of patent grafts. '°V ariant angina is caused by coronary spasm, but the cause of spontaneous coronary spasm is unclear.…”

mentioning

confidence: 99%

Percutaneous transluminal coronary angioplasty in patients with variant angina.

Planchard¹,

Waters²,

Scholl³

et al. 1982

Circulation

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SUMMARY Among the first 83 patients treated with percutaneous transluminal coronary angioplasty (PTCA) at our institution, typical variant angina was recognized beforehand in five cases and was discovered within 4 months of PTCA in six others. All patients had a 65-95% proximal left anterior descending coronary artery stenosis and only one had a coronary lesion >50% in other coronary arteries. Before PTCA, all patients were premedicated with calcium-antagonist drugs. Thirteen of 15 PTCAs, including three of four repeat PTCAs, were technically successful. However, variant angina recurred after successful PTCA in three of the five patients in whom it was documented beforehand and in an additional two of two patients with variant angina before a successful repeat PTCA. Overall, among the nine patients with variant angina after successful PTCA, five had restenosis at the site of PTCA and two others developed severe lesions adjacent to the site of PTCA within 4 months of the procedure. The three patients without restenosis have been treated with calcium-antagonist drugs from soon after PTCA and have remained angina-free.These results suggest that PTCA is technically feasible in patients with variant angina who have organic lesions, but symptoms due to coronary spasm usually persist or recur, often with restenosis.

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“…There is good experimental evidence indicating that bilateral sympathectomy can protect against arrhythmias (2) and that left stellate ablation, in contrast to the arrhythmic right stellectomy (28), will diminish ventricular arrhythmias and ventricular fibrillation associated with acute myocardial ischemia (28,29). More recently, selective cardiac denervation has been performed in patients undergoing multiple vessel bypass surgery (2,3) and it appears that the procedure brought added therapeutic benefits (2,3).…”

Section: Discussionmentioning

confidence: 99%

“…More recently, selective cardiac denervation has been performed in patients undergoing multiple vessel bypass surgery (2,3) and it appears that the procedure brought added therapeutic benefits (2,3). On the other hand, since it is now well established that in cases of sinus node default, escape and maintenance of subsidiary atrial pacemaker activity and AV junctional automaticity are both critically dependent upon sympathetic input, caution should be exercised when considering a therapeutic left stellectomy particularly in those patients who have known or suspected sinus node disorders.…”

Section: Discussionmentioning

confidence: 99%

Differential effects of sympathetic activity on AV junctional automaticity and AV conduction

et al. 1986

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Rapid ventricular response during episodes of supraventricular tachycardia are often followed, on abrupt cessation of the tachycardia, by prolonged pauses terminated by a sluggish and sometimes erratic escape of a supraventricular pacemaker. Such chronotropic-dromotropic paradoxes are readily reproduced in the animal laboratory following elimination of the sinus node and bilateral decentralization of the stellate ganglia and vagi. This study examined whether left stellate stimulation (0.5, 1, 2, 4, 8 and 16 Hz) or lack thereof differentially affected AV junctional automaticity and AV conduction. In the absence of any sympathetic neural activity (maximal sympathetic deficit), the AV junctional rate averaged a mere 22 +/- 2 percent of its peak performance, whereas under the same conditions, anterograde AV conduction averaged 73 +/- 5 percent and retrograde VA conduction 56 +/- 13 percent of their respective peak performances. On comparing the response curve (normalized responses) for AV junctional automaticity with that obtained for anterograde AV conduction the differences were significant at all frequencies between 0 and 4 Hz. Retrograde VA conduction (as assessed by the fastest ventricular pacing rate still conducted 1:1 to the atria) was always significantly less than anterograde AV conduction (as assessed by the fastest atrial pacing still conducted 1:1 to the ventricles). These results indicate that AV junctional automaticity is considerably more affected by sympathetic deficit than are either anterograde or retrograde AV conduction. In other words, AV junctional automaticity is far more dependent upon sympathetic input than AV conduction. While sympathetic influence is critical to the escape and maintenance of AV junctional automaticity both anterograde and retrograde AV conduction are remarkably resilient even under conditions of severe sympathetic deficit.

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Surgical treatment of variant angina: use of plexectomy with aortocoronary bypass.

Cited by 63 publications

References 15 publications

Coronary artery spasm

Coronary artery spasm

Percutaneous transluminal coronary angioplasty in patients with variant angina.

Differential effects of sympathetic activity on AV junctional automaticity and AV conduction

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