Spasm in Arterial Grafts in Coronary Artery Bypass Grafting Surgery.

Spasm of arterial grafts in coronary artery bypass grafting surgery is still a clinical problem, and refractory spasm can occasionally be lethal. Perioperative spasm in bypass grafts and coronary arteries has been reported in 0.43% of all coronary artery bypass grafting surgery, but this may be an underestimate. Spasm can develop not only in the internal mammary artery but more frequently in the right gastroepiploic and radial artery. The mechanism of spasm can involve many pathways, particularly those involving regulation of the intracellular calcium concentration. Endothelial dysfunction also plays a role in spasm. Depending on the clinical scenario, the possibility of spasm during and after coronary artery bypass grafting should be confirmed by angiography. If present, immediate intraluminal injection of vasodilators is often effective, although other procedures such as an intraaortic balloon pump or extracorporeal membrane oxygenation may also become necessary to salvage the patient. Prevention of spasm involves many considerations, and the principles are discussed in this review article.

Intermediate fixed coronary artery stenosis at the site of ergonovine-provoked spasm as a predictor of long-term major adverse cardiac events of patients with coronary spastic angina.

BACKGROUND: Organic coronary artery stenosis is a significant prognostic factor in patients with coronary spastic angina (CSA), so the present study was focused on assessing the impact of intermediate fixed stenosis at sites of provoked spasm on the long-term outcomes of CSA patients. METHODS AND RESULTS: CSA patients diagnosed on the basis of ergonovine-provoked spasm were enrolled and the clinical background and long-term prognosis of CSA patients with intermediate fixed stenosis at the site of provoked spasm (with-fixed-stenosis group, n=37) and those without fixed stenosis (without-fixed-stenosis group, n=126) were retrospectively compared. During the follow-up period (average 4.01 years for with-fixed-stenosis, 4.47 years for without-fixed-stenosis), the with-fixed-stenosis group had a significantly lower event-free survival rate, as well as a higher frequency of admission for unstable angina and percutaneous coronary intervention than the without-fixed-stenosis group, whereas the survival rate did not differ significantly between the 2 groups. In the multivariate analysis, intermediate fixed stenosis at the site of provoked spasm was a predictor of long-term major adverse cardiac events (MACE). CONCLUSIONS: Intermediate fixed stenosis at the site of ergonovine-provoked spasm is an independent risk factor for MACE during the long-term period in CSA patients.

Intrathecal baclofen for spasticity of spinal origin: seven years of experience.

A total of 66 consecutive patients with severe spasticity of spinal cord origin were screened with intrathecal baclofen, and all but two responded with a two-point decrease in their Ashworth spasticity scale and/or spasm scale score. Of these, 62 elected to receive chronic intrathecal baclofen administration by means of an implanted delivery system. These patients have been followed for an average of 30 months (the first three for 81 months). Intrathecal baclofen has been well tolerated and all serious side effects were transient and have been managed by dose adjustments. The pump presently available has worked safely; the only problem has been stalling in 7% of these devices. The catheter system has had to be repaired in just over one-half of the patients and is the main cause of interruption of drug delivery. Of the 62 patients implanted, 52 (84%) continue to be treated adequately for spasticity; there are three poor long-term responders, four deaths due to underlying disease, and three whose participation has been voluntarily withdrawn. It is suggested that long-term control of spinal spasticity by intrathecal baclofen can be achieved in most patients.

Agonal hepatic arterial vasospasm.

The effect of donor pretreatment with Dibenzyline (phenoxybenzamine) on hepatic arterial vasospasm was studied in a porcine asphyxia model. Nine pigs underwent hepatectomy without pretreatment, while six were given 2 milligrams per kilogram of Dibenzyline prior to hepatic dissection. Hepatic arterial blood flow was monitored with an electromagnetic flow probe, and after cardiac arrest, arteriograms of the hepatic circulation were obtained. Hepatic arterial vasospasm occurred in seven of the pigs in group 1 and in only one of group 2 (p less than 0.05). Agonal hepatic arterial blood flow remained constant (415 +/- 30 milliliters per minute) in pretreated pigs during asphyxia, but was markedly reduced (98.6 +/- 63.3 milliliters per minute) in nonpretreated pigs (p less than 0.05). Results of this study demonstrate the agonal occurrence of hepatic arterial vasospasm and its prevention with Dibenzyline. Donor pretreatment with alpha-adrenergic antagonists may be indicated in clinical organ procurement to prevent agonal arterial vasospasm and its potentially adverse effect on early hepatic allograft function.

On the mechanism of sudden death in Moersch-Woltman syndrome.

A patient dying in the hospital with Moersch-Woltman Stiff-person syndrome (MWS) suffered from episodic, severe, uncompensated metabolic acidosis. Possible explanations for the acid-base abnormalities in this neurologic disorder are proposed.