[Clinical considerations in percutaneous transluminal coronary angioplasty].
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Angioplasty, Balloon, Coronary↗
Biomedical subjects
M Mosseri
Publications and source records attributed to M Mosseri.
[The vascular stent in percutaneous coronary revascularization].
Balloon angioplasty is commonly used for coronary revascularization. Coronary stents were introduced to overcome its 2 main limitations: acute coronary occlusion and restenosis. We describe our experience with the use of 27 coronary stents in 26 patients. The indications for stenting were acute or threatened coronary occlusion in 16 patients, in 7 recurrent restenosis, and vein graft narrowing in the rest. Stent deployment was successful in all cases and there was no mortality. The hospital course was complicated by subacute thrombotic occlusion of the stent (2 patients) initially treated by balloon angioplasty, retroperitoneal bleeding (3), and surgical closure of femoral pseudoaneurysm (2); 22 were discharged without complications; 1 patient required coronary bypass. Coronary stenting has a high rate of success and is very effective in cases of abrupt coronary occlusion which would otherwise require emergency surgery. It is probably associated with a lower restenosis rate than standard balloon angioplasty. Accurately monitored anticoagulant therapy is essential to prevent complications.
Angioplasty, Balloon, Coronary↗
Prolonged postoperative myocardial ischaemia and infarction in vascular surgery performed under regional anaesthesia.
The importance of prolonged postoperative myocardial ischaemia in cardiac outcome has recently been emphasised. The present study examines the correlation between perioperative ischaemia and myocardial infarction (MI) in patients undergoing peripheral vascular surgery (PVS) under regional anaesthesia. One-hundred-and-forty consecutive peripheral vascular operations under regional anaesthesia were prospectively analysed, using Holter monitoring for perioperative myocardial ischaemia (defined as down sloping or horizontal ST-segment depression of > or = 1 mm) and postoperative cardiac outcome. The study was approved after informed consent. There were 82 carotid endarterectomies under cervical block and 58 infrainguinal bypass procedures under continuous spinal or epidural anaesthesia. IHD was present in 53.6% cases: previous MI-38%; angina pectoris-33%; previous CABG/PTCA-24%. Holter monitoring started about 20 hours before surgery and continued for 45 hours. After surgery patients were followed for signs of cardiac complications; daily 12 lead ECG; 6 hourly CK-MB isoenzymes during the first 24 postoperative hours and later whenever indicated. MI diagnosis was based on chest pain, permanent new ECG changes and CK-MB elevation. There was no 30-day mortality. Postoperative MI occurred in seven patients (5%). Five of the postoperative MI were non-Q-wave infarctions. The majority (71%) of the adverse cardiac events started within 24 hours of surgery, and the latest occurred 52 and 72 hours post surgery. In 65 cases (46.4%) there were 259 episodes of significant ST-depression. In 75 (53.6%) cases ischaemic episodes were not detected. Patients with postoperative cardiac events had significantly more and longer ischaemic episodes in all three perioperative periods than those without such events.(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗
Total coronary artery occlusion late after successful coronary angioplasty of moderately severe lesions: incidence and clinical manifestations.
Coronary restenosis after balloon angioplasty is a slow process that develops over a few months. In some patients, with an initially successful angioplasty, an artery that originally had only moderate stenosis becomes totally occluded as a result of restenosis. This report describes 16 such patients out of 415 dilated lesions with late angiographic follow-up. Ten patients presented with stable angina pectoris, 5 had unstable angina and only one was admitted with a small myocardial infarction. Visible collaterals were present in 15 patients. Except for the patient who sustained myocardial infarction, none of the late angiograms showed the typical morphological features of acute lesion. We conclude that total coronary occlusion late after successful angioplasty of an artery that was moderately narrowed is rare. The 'restenotic' occlusion is a slow process that stimulates collateral formation and thus the risk of myocardial infarction is small.
Adult↗
Very early thrombolysis in acute myocardial infarction--a light at the end of the tunnel.
Myocardial damage in acute myocardial infarction is a time-dependent process. Thrombolytic therapy effectively opens the coronary artery, restores coronary blood flow and prevents ongoing necrosis. We examined the effect of very early thrombolytic therapy (including prehospital administration) in a consecutive group of 510 patients with myocardial infarction on the following factors: mortality, complications and the preservation of left ventricular function. The treatment was given to 89 at home (time delay to treatment 1.2 +/- 0.6 h) and 421 in hospital (2.0 +/- 1.0 h). Twelve patients died in hospital and major hemorrhage occurred in 10. The arterial patency rate in 416 patients who underwent coronary angiography 6 days later was 82%. Infarct size measured by left ventriculography was determined by the area at risk, the delay time until the initiation of thrombolytic therapy, the total duration of ischemic pain and the degree of restoration of arterial blood flow. We conclude that early thrombolytic therapy, particularly prehospital management, is feasible and safe and reduces infarct size and mortality. A further decrease in the delay to initiation of treatment and more effective thrombolytic therapy will further decrease mortality and myocardial damage.
Aged↗
In vitro evidence that myocardial ischemia resulting from 5-fluorouracil chemotherapy is due to protein kinase C-mediated vasoconstriction of vascular smooth muscle.
5-Fluorouracil (5-FU) is a commonly employed chemotherapeutic agent. Among the various toxicities associated with 5-FU, cardiovascular toxicity, consisting principally of acute myocardial ischemia and/or myocardial infarction, has been reported in up to 8.5% of patients treated with this drug. While 5-FU-induced coronary vasospasm has been considered as a potential basis for such clinical toxicity, this hypothesis remains unsubstantiated by laboratory investigation. Accordingly, the present study was designed to investigate the hypothesis that 5-FU induces reversible vasoconstriction of vascular smooth muscle and to study the cellular mechanisms of such vasomotor alterations. To investigate the effects of 5-FU on the vasoreactivity of vascular smooth muscle, 479 exposures were performed in 105 rings of aorta freshly isolated from 23 New Zealand white rabbits. Vasoconstriction was documented in 20 of 86 (23%) rings exposed to 5-FU at 7 x 10(-5) M, 45 of 83 (54%) rings exposed to 5-FU at 7 x 10(-4) M, and 41 of 49 (84%) rings exposed to 5-FU at 7 x 10(-3) M. In each case, 5-FU-induced vasoconstriction was endothelium independent. Pretreatment of rings with 10(-9) M staurosporine, a protein kinase C (PK-C) inhibitor, reduced 5-FU-induced vasoconstriction from 25.0 +/- 6.5 to 2.5 +/- 1.7 mg; staurosporine at a concentration of 10(-8) M abolished 5-FU-induced vasoconstriction. Pretreatment of rings with 10(-7) M phorbol-12,13-dibutyrate, an activator of PK-C, increased the magnitude of 5-FU-induced vasoconstriction 23-fold, from 49.7 +/- 11.1 mg before to 1163.6 +/- 276.4 mg after phorbol-12,13-dibutyrate (P = 0.0002). Neomycin, an inhibitor of phosphoinositide turnover, did not alter the magnitude of 5-FU-induced vasoconstriction. Membrane receptor blockers, including the alpha-adrenergic receptor blocker phentolamine, the beta-adrenergic receptor blocker propranolol, the H1 receptor inhibitor diphenhydramine, the H2 receptor inhibitor cimetidine, the Ca2+ channel blockers verapamil and diltiazem, and the cyclooxygenase inhibitor indomethacin all failed to alter the magnitude of 5-FU-induced vasoconstriction. Furthermore, the 5-FU-related compounds uracil and floxuridine did not produce vasoconstriction. Finally, 5-FU-induced vasoconstriction was abolished by nitroglycerin. These results indicate that (a) 5-FU causes direct, endothelium-independent vasoconstriction of vascular smooth muscle in vitro, (b) this vasomotor response involves activation of PK-C, and (c) this response is independent of vasoactive cell membrane receptors, phosphoinositide turnover, or activation of the cyclooxygenase pathway.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
[Advances in percutaneous coronary revascularization].
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Angioplasty, Balloon, Coronary↗
Importance of long-duration postoperative ST-segment depression in cardiac morbidity after vascular surgery.
Major vascular surgery is associated with a high incidence of cardiac ischaemic complications. By means of continuous perioperative electrocardiographic recording, we studied 151 consecutive patients undergoing major vascular surgery to find out the characteristics of any myocardial ischaemia and the relation to outcome. 13 (8.6%) patients had postoperative cardiac events (6 myocardial infarctions, 2 unstable angina, and 5 congestive heart failure). There were 342 perioperative ischaemic episodes shown by ST-segment depression; 164 (48%) occurred postoperatively. Postoperative ischaemic episodes were significantly longer than episodes before or during operations (3.2 vs 1.7 and 1.5 min per h monitored, respectively, p < 0.001). Both Detsky's cardiac risk index and long-duration (> 2 h) preoperative ischaemia were predictive of postoperative cardiac complications (odds ratios in univariate analysis 3.3, p = 0.03, and 7.2, p = 0.009, respectively). However, long-duration (> 2 h) postoperative ischaemia was the only factor significantly associated with cardiac morbidity in multivariate logistic regression analysis (odds ratio 21.7, p = 0.001). Long-duration ST-segment depression preceded most (84.6%) postoperative cardiac events, including myocardial infarctions, and no cardiac event was preceded by ST-segment elevation. 5 of the 6 postoperative myocardial infarctions were non-Q-wave infarctions. We conclude that long-duration subendocardial ischaemia, rather than acute coronary artery occlusion, may bring about postoperative myocardial injury and complications.
Aged↗
Arterial remodelling after percutaneous transluminal balloon angioplasty.
Atheromatous coronary artery disease progresses by atheroma accretion, plaque rupture and thrombus formation, with or without spontaneous fibrinolysis. The natural history may be altered by modifying risk factors in an attempt to induce regression, or treated by mechanical means such as balloon angioplasty, directional coronary atherectomy or drills, or flow modulated by the insertion of an aorto coronary bypass graft with or without endarterectomy. Here we discuss the natural history of the atheromatous disease in a series of 355 patients who underwent at least one PTCA procedure and then underwent a second angiographic study to determine the changes in the dilated and nondilated arteries.
Angioplasty, Balloon, Coronary↗
Inhibition of endothelium-dependent vasorelaxation by sickle erythrocytes.
Interactions between erythrocytes and vascular endothelium have been implicated in the pathogenesis of vaso-occlusion in sickle cell anemia. Sickle erythrocytes adhere to endothelial cells and facilitate trapping of rigid sickle cells in microvessels. Compensatory dilation of precapillary arterioles may mitigate the occlusion. The endothelium regulates vasoreactivity by elaborating endothelium-derived relaxing factor (EDRF), a small molecule that passes freely into vascular smooth muscle where it initiates vasorelaxation by activating soluble guanylate cyclase in the smooth muscle cell cytoplasm. Endothelial release of EDRF can be stimulated by agonists such as acetylcholine. It is highly sensitive to decomposition by superoxide anions and is rapidly bound and inactivated by oxyhemoglobin in solution. The purpose of this study was to determine whether sickle cell interaction with endothelium disrupts this mechanism of endothelial regulation of vasomotor tone. Transverse strips of rabbit aorta, mounted isometrically in organ baths, were contracted with norepinephrine, and relaxation responses to acetylcholine or other agonists were determined. Responses were measured under control conditions and again in the presence of oxyhemoglobin A or S, or erythrocytes or ghosts from normal control subjects or patients with homozygous sickle cell anemia. Sickle erythrocytes inhibited vasorelaxation to acetylcholine by 83%. Approximately half of the inhibition was attributable to a small amount of oxyhemoglobin S that was leaked into the buffer from the erythrocytes. Consistent with this, sickle erythrocyte ghosts inhibited vasorelaxation to acetylcholine by up to 45%. Ghosts from normal erythrocytes did not inhibit vasorelaxation to acetylcholine, and the inhibition seen with normal erythrocytes was entirely attributable to leakage of oxyhemoglobin A into the bath buffer.(ABSTRACT TRUNCATED AT 250 WORDS)
Acetylcholine↗
Excimer laser-induced vasoreactivity.
Earlier generations of excimer lasers, designed for industrial or non-cardiovascular medical applications, have been previously shown consistently to induce vasorelaxation of vascular smooth muscle in vitro. Such lasers were typically characterized by pulse durations of < or = 15 nanoseconds (ns). Excimer lasers currently employed for cardiovascular applications were designed with longer pulse durations (up to 220 ns) to facilitate fibreoptic transmission. Because arterial spasm has been observed in patients undergoing percutaneous revascularization with such lasers, we investigated the effect of so-called 'stretched pulse' excimer laser irradiation on vasomotor reactivity. A total of 69 rings of aorta harvested from New Zealand white rabbits were mounted isometrically in Krebs buffer solution and exposed to 308 nm from an excimer laser with a pulse duration of 120 ns. Fifty rings were exposed without pharmacological pre-treatment. The remaining 19 rings were exposed after pharmacological pre-treatment: 11 were precontracted with norepinephrine (NE, 10(-9)-10(-5) M), while eight were irradiated in Ca(2+)-free buffer after pre-relaxation with nitroglycerin (NTG, 7 x 10(-5) M). Without pharmacological pre-treatment, the vasomotor response to the excimer laser was variable: vasoconstriction was observed in 27 rings (16.1 +/- 0.8% (mean +/- SEM) of response to 5-HT), vasorelaxation in 21 rings (43.2 +/- 17.0% of response to 5-HT), and a heterogeneous response (vasoconstriction 4.9 +/- 1.0%, vasorelaxation 12.9 +/- 0.3%) in two rings. The vector of vasomotor response in non-precontracted rings was not predicted by fluence, frequency or temperature rise. A consistent vasomotor response was recorded only when pharmacological pre-treatment was employed. Among 11 rings pre-contracted with NE, the excimer laser produced vasorelaxation in 34/34 (100%) exposures; in contrast, among eight rings pre-relaxed with NTG in Ca(2+)-free buffer, the excimer laser produced vasoconstriction in 40/40 (100%) exposures. For all rings, including pre-contracted, pre-relaxed and those which were not pharmacologically pre-treated, the vector of vasomotor response was endothelium-independent. The magnitude of all vasomotor responses, including vasoconstriction in non-precontracted rings, could be diminished by limiting the duration of exposure. Thus, in contrast to the earlier generation, short-pulse excimer lasers, long pulse-duration excimer lasers in current clinical trials produce an unpredictable, heterogeneous vasomotor response. This in-vitro finding is consistent with the unpredictable development of vascular spasm in patients undergoing excimer laser angioplasty. Furthermore, these findings support the concept of employing abridged pulse trains to diminish the likelihood of laser-induced vasoconstriction during excimer laser angioplasty.(ABSTRACT TRUNCATED AT 400 WORDS)
Angioplasty, Laser↗
Laser-tissue interactions: vascular reactivity.
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Animals↗
Angiographic findings in the coronary arteries after thrombolysis in acute myocardial infarction.
The angiographic appearance of the coronary arteries was examined in 308 patients with acute myocardial infarction (AMI) who received high-dose intravenous thrombolytic therapy. Coronary angiography was performed on day 7 after admission to the hospital. Patients had an average of 2.4 discrete arterial narrowings or obstructions. The narrowings were proximal and related to bifurcations. Four fifths of the culprit arteries were patient; 104 (34%) had a ruptured plaque, 22 (7%) had an ulcerated plaque, and in 190 (62%) the lesions were eccentric. Patients differed from a comparable, previously studied, control series of 302 patients with chronic stable angina pectoris who had more extensive disease. They had 5.7 narrowings/patient, also located proximally and at bifurcations, but more widely distributed in the coronary tree. Patients with AMI who are suitable for thrombolysis have a unique coronary angiographic picture. The data confirm that AMI is caused by sudden rupture of a localized atheromatous plaque that initiates an obstructive thrombotic cascade.
Angina Pectoris↗
Laser-induced dissections: pathogenesis and implications for therapy.
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Angioplasty, Laser↗
Immunohistochemical evidence for IgA1 involvement in Graves ophthalmopathy.
Orbital muscle, adipose tissues, and periorbital muscle from 11 patients with Graves ophthalmopathy were studied with in situ assays using monoclonal antibodies for IgA1, IgA2, IgM, and IgG. Tissue biopsies were taken from varied extraocular muscles and orbital sites. All cases were from patients with severe disease or disease of long duration. Control specimens of extraocular muscle tissues were obtained from nine patients treated for unrelated orbital disorders. Only connective tissue associated with the extraorbital muscles and periorbital muscles showed any reactivity. Of the muscle tissue obtained from patients with Graves disease all exhibited IgA1 positive staining of the endomysium and perimysium, without staining of the muscle fibers themselves. Parallel sections of orbital muscles reacted with anti-IgA2 or anti-IgM antibody failed to demonstrate staining. Control extraocular muscle tissue did not stain with anti-IgM and one control muscle of seven reacted minimally with anti-IgA2. Some reactivity with anti-IgA1 was seen in four of the seven control muscles but this was qualitatively much less than that of muscle tissue from patients with Graves disease. Monoclonal anti-IgG did not stain tissue from the six Graves specimens and three control specimens tested.
Adipose Tissue↗
Percutaneous delivery of low-level laser energy reverses histamine-induced spasm in atherosclerotic Yucatan microswine.
BACKGROUND: Previous in vitro experiments performed in our laboratory have shown that low-level laser energy may produce prompt reduction in isometric tension of vascular smooth muscle. The present study was designed to extend these previous in vitro findings to an in vivo model and thereby investigate the hypothesis that laser light delivered percutaneously in vivo could successfully reverse arterial spasm. METHODS AND RESULTS: Spasm defined as greater than 50% reversible reduction in luminal diameter persisting for greater than or equal to 5 minutes was successfully provoked by injection of histamine (100-400 micrograms/kg) in 13 arteries among 10 atherosclerotic Yucatan microswine; the magnitude of histamine-induced vasoconstriction was then documented angiographically by repeated injections of contrast media for as long as 30 minutes (controls). After return of angiographic luminal diameter to baseline, spasm was reproduced with a second injection of histamine into the same artery. Representative wavelengths generated by ultraviolet (UV), visible, and infrared lasers were then delivered percutaneously via conventional fiberoptics to the site of spasm, and angiographic assessment was repeated for as long as 30 minutes (treatment trial). In three arteries treated with UV (351 nm) light from an excimer laser, angiographic luminal diameter narrowing decreased from 100% to 23.9%, 50.0% to 9.3%, and 76.0% to 42.3%, respectively. The magnitude of laser-induced increase in luminal diameter was 50.2 +/- 22.7%, which was significantly greater than the magnitude of relaxation observed spontaneously during the control trials (10.9 +/- 9.8%, p = 0.02). Visible light from a helium-neon (632 nm) laser accomplished complete reversal of histamine-induced spasm in two of four arteries; in the remaining two arteries, luminal diameter narrowing percentages were reduced from 57.0% to 20.0% and from 76.5% to 30.8%, respectively. The magnitude of helium-neon laser-induced relaxation (55.8 +/- 17.9%) was again significantly greater than that observed during the control trials (0.9 +/- 1.9%, p = 0.01). Finally, infrared irradiation from a diode-pumped neodymium:yttrium aluminum garnet (1,064 nm) laser decreased histamine-induced luminal diameter narrowing in three arteries from 100% to 21.4%, 56.0% to 8.7%, and 68.3% to 35.3%, respectively. The magnitude of infrared laser-induced improvement in luminal diameter narrowing was 53.0 +/- 23.3%, which was significantly greater than that observed during the control trials (12.9 +/- 10.7%, p = 0.01). In three additional arteries, fiberoptic sham trials (without laser irradiation) failed to produce relaxation of histamine-induced spasm. CONCLUSIONS: These findings document for the first time that light-induced relaxation of vascular smooth muscle, previously documented in vitro, may be reproduced in vivo.
Animals↗
Coronary pathology predicts conduction disturbances after coronary artery bypass grafting.
Conduction disturbances after coronary artery bypass grafting may result from compromised septal blood flow. To examine this hypothesis we reviewed the preoperative coronary angiography of 55 consecutive patients undergoing coronary artery bypass grafting. Thirty-five patients had either no lesion or a discrete lesion in the left anterior descending coronary artery that did not include the septal perforator (type I anatomy). Twenty patients had a lesion of the left anterior descending coronary artery at the origin of the first septal branch, a lesion of the first septal artery, or a pair of lesions in the left anterior descending coronary artery that straddled the origin of the first septal artery; all lesions were proximal to the graft site (type II anatomy). None of the patients with type I anatomy had a major conduction disturbance after coronary artery bypass grafting. Eleven of the patients with type II anatomy had major conduction disturbances after coronary artery bypass grafting; right bundle-branch block in 1, right bundle-branch block and left anterior hemiblock in 2, left bundle-branch block in 5, and complete atrioventricular block that required pacemaker implantation in 3 (p less than 0.001). In the 20 patients with type II anatomy, the appearance of conduction disturbances correlated well with the absence of retrograde flow to the septal branches from the right coronary artery (p less than 0.01). Pathological lesions in the left anterior descending coronary artery that compromise flow in the first perforator and that do not provide an adequate circulation produce localized damage and conduction disturbances after coronary artery bypass grafting. This can be predicted from the preoperative angiographic anatomy.
Aged↗
Maturation of the contralaterally recorded auditory brain stem response.
Ipsilaterally and contralaterally recorded auditory brain stem responses to 80 dB nHL clicks were recorded from 37 infants, aged 2 weeks to 20 mo and from six adults, all with normal auditory function. With increasing age, contralateral waves A, B, C, and D and ipsilateral waves III and V decreased in latency, with the contralateral morphology more closely resembling the ipsilateral morphology as age increased, especially after the age of 9 mo. The mean latencies and their change with age for waves A and B resembled those of ipsilateral waves III and III', respectively; both waves C and D demonstrated similarities with wave V. Large waveform changes were seen with maturation in the latency region of contralateral waves C and D. In 42 of 43 subjects, wave V latency occurred after wave C and before wave D. Peak to peak amplitudes of contralateral waves A-B and D-E' increased with age, but were smaller than those of ipsilateral I'-III and V-V', respectively. The smaller contralateral responses make their use for threshold estimation problematic, especially before the age of 9 months. The contralateral response, however, may help to select wave V in ambiguous cases, and to determine response laterality.
Acoustic Stimulation↗