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Background Participation rates of patients with acute coronary syndrome (ACS) in efficacious cardiac prevention and rehabilitation programmes (CPRPs) are low, particularly in ethnic minorities. Few studies have evaluated the full array of potential barriers to participation in a multiethnic cohort with identical insurance coverage. Objective To assess the hierarchy of multiple barriers (ie, sociodemographic, systemic, illness related, psychological and cultural) to participation in CPRP of Jewish and Arab patients served by a regional hospital in Israel. Methods Patients with ACS (N=420) were interviewed during hospitalisation about potential barriers and subsequently about participation in CPRP. Decision tree analysis determined, hierarchically, the best predictors of participation in CPRP. Results Ethnicity was the salient predictor of participation in CPRP (61.1% (95% CI 55.6% to 66.5%) of Jewish patients versus 17.2% (95% CI 11.2% to 24.9%) of Arab patients). Among Jewish patients the dominant determinant was a recommendation for CPRP in the hospital discharge letter (32.5% (95% CI 23.1% to 43.1%) vs 71.9% (95% CI 65.8% to 77.6%) participation without and with a recommendation, respectively). Other major hierarchical determinants included age, discharge diagnosis, socioeconomic position and perceived benefits of exercise. Among Arab patients, anxiety was the main predictor (5.5% (95% CI 1.1% to 14.1%) vs 27.9% (95% CI 17.7% to 40.0%) participation among those with high vs lower anxiety levels). Additional contributors were a predischarge visit to the rehabilitation centre (familiarisation) and car ownership (access). Conclusions Utilisation of decision tree analysis enables us to identify the key barriers to participation in CPRP in an ethnic-specific mode. Interventions to improve participation can then be designed to address each group9s specific barriers.

Background and Purpose —Long-term survival in patients after carotid endarterectomy (CEA) is determined mainly by their concomitant cardiac disease. We tested to determine whether preoperative thallium scanning (PTS) and subsequent selective coronary revascularization (CR), by either percutaneous transluminal coronary angioplasty (PTCA) or coronary artery bypass grafting (CABG), improve long-term survival after CEA. Methods —Two hundred twenty-six of 255 consecutive patients (88%) undergoing CEA from 1990 to 1996 had PTS. Those with significant reversible defects on PTS were referred for coronary angiography and possible CR. Patients who had undergone PTS were divided into the following 4 groups: group 1, normal or mild defects on PTS; group 2, moderate-severe fixed and/or reversible defects in patients who did not undergo CR; group 3, patients who had CR secondary to their PTS results; and group 4, patients who had CR in the past that was not related to the PTS. Perioperative data were prospectively recorded, and data on long-term survival and cardiac and neurological complications were collected. Results —Seventy-seven patients (34%) had preoperative coronary angiography, and 42 (19%) had subsequent CR: preoperative PTCA or CABG in 24, combined CEA+CABG in 10, and post-CEA CABG in 8 patients. No deaths resulted from the coronary angiography, CR, or CEA. Six patients had perioperative nonfatal myocardial infarction and 8 had stroke. During the follow-up (40±23 months), 47 patients (18%) died, 31 (66%) from cardiac disease and 4 (8.5%) from stroke. Independent predictors of long-term overall mortality were diabetes mellitus, preoperative T-wave inversion on ECG, lower-extremity arterial disease, and history of neurological symptoms [exp(β)=3.5, 3.4, 2.5, and 2.4; P =0.0003, 0.0004, 0.01, and 0.04, respectively]. In addition, preoperative moderate-severe thallium defect without CR (group 2) independently predicted long-term cardiac mortality [exp(β)=2.8; P =0.04]. Patients with preoperative CR (group 3) had long-term survival rate similar to that of group 1 and significantly better than that of group 2 ( P =0.02). Conclusions —PTS predicts long-term survival, and selective CR based on the thallium results improves the survival rate of patients undergoing CEA.

A small gap between stent struts is essential to support the vessel wall, prevent elastic recoil, and prevent intimal flaps from prolpasing into the lumen. We defined Gap Index as the ratio of strut width divided by the percent of the vessel wall area covered by the stent metal, and proved mathematically that this index relates inversely to the total length of stent struts (or coil), and directly related to stent cell size. Twenty-four (12 tubular and 12 coil) stents from 17 manufacturers were analyzed. Strut width in the tubular and coil groups was 354.1 +/- 276.0 and 955.9 +/- 553.9 microm, respectively (P < 0.001). The relative metallic surface area (RMS) in the tubular and coil groups for 3 mm stent diameter was 16.0 +/- 4.6 and 10.6 +/- 3.7%, respectively (P < 0.005). Great variations in Gap Index were found amongst different stents, with up to 100-fold. Gap Index in the tubular and coil groups for 3 mm stent diameter was 24.4 +/- 21.7 and 105.8 +/- 97.5 units, respectively (P = 0.001). Thus, coil stents have a smaller relative metallic surface area despite increased strut width. This is the result of reduced total strut length and fewer and larger cells, as represented by a higher Gap Index. This information may be useful for new stents designs.

The initial experience with the use of long coronary stents (> 30 mm in length) was analyzed retrospectively. Sixty-seven stents were deployed in 58 narrowings in 57 patients (34 AVE Microstents, 16 Nir stents, four Gianturco-Roubin II stents, and 13 Wallstents). Stents were implanted in 22 patients with unstable angina, 34 patients with stable angina, and one patient during direct angioplasty for acute myocardial infarction. Eighteen additional short stents were implanted to cover the entire length of the lesions so that an average of one and a half stents were deployed per patient. The length of the narrowings before stenting was 40 +/- 20 mm and the length of the stented segments was 45 +/- 20 mm. Stents were deployed for "bailout" in 23 narrowings, to improve suboptimal results of balloon angioplasty in 18 narrowings, and electively in 17 narrowings. Twenty of the 67 long stents were deployed in saphenous vein grafts. The success rate of stent implantation was 100%. One patient had a rupture of a saphenous vein graft after deployment of two long stents, with tamponade treated by emergency surgery. One patient had chest pain 18 hours after stent deployment; by the time he arrived at the catheterization laboratory the pain had subsided and the angiogram revealed a patent artery with normal flow. There were no other major complications during the hospital course and 1-month follow-up. We conclude that long coronary stents can be deployed successfully in native coronary arteries and vein grafts. They are useful for elective implantation and extremely helpful in bailout situations. The immediate results are excellent, but long-term outcome is awaited.

We evaluated the long-term angiographic outcome of balloon angioplasty by comparing original and follow-up target coronary narrowing. Rather than using restenosis to determine outcome, as in most angioplasty studies, we took an unusual approach and analyzed outcome in terms that are commonly used in progression and regression studies after medical interventions. Quantitative angiographic measurements were undertaken in 315 narrowings with an initial diameter stenosis90% before and after angioplasty and at follow-up. Angiographic deterioration (10% increase in follow-up diameter stenosis) was identified in 44 (14%) narrowings. Angiographic deterioration was not influenced by age, sex, risk factors, lipid profile, or the indication for angioplasty. Deterioration was also not predicted by the severity, length, or the location of the narrowing. The deteriorating narrowings had a higher recoil after dilatation compared with narrowings with angiographic improvement (21% +/- 31% vs 12% +/- 17%, p = 0.006); the residual stenosis after angioplasty was therefore higher. The late loss was also significantly increased compared with narrowings with angiographic improvement (65% +/- 26% vs 8% +/- 24%, p0.001). We conclude that the incidence of angiographic deterioration of coronary disease as a result of restenosis is uncommon but not negligible. Interventional cardiologists should resist the temptation to dilate mild, silent coronary narrowings because the procedure might have an unfavorable angiographic (and probably clinical) effect.

Intravascular ultrasound (IVUS) is a new technique of tomographic visualization of the coronary arteries: its lumen, wall and pathology. Three dimensional (3D) reconstruction shows the tubular structure of the arterial wall and its pathology. IVUS has many advantages over coronary angiography: it has better resolution and shows many hidden lesions. IVUS has helped uncover the underlying mechanisms of percutaneous transluminal coronary angioplasty (PTCA), restenosis, the use and value of other interventional techniques such as directional coronary atherectomy (DCA), rotational atherectomy and stent implantation, and has great value in planning complex interventional procedures. The new American Heart Association (AHA) classification of coronary atherosclerosis pathology can be demonstrated by IVUS. IVUS is sensitive for studies of atheroma regression and progression and shows the coronary artery lesions after cardiac transplantation.

Revascularization is a theoretically ideal technique for treating repeated angina pectoris in elderly patients. Coronary angioplasty is an attractive option if it can be performed safely. In this report, we describe our experience with 80 angioplastic procedures in 72 patients older than 80 years. Seventy-two of these procedures (90%) were performed after 1990 using the currently available, improved angioplasty equipment. A third of these patients did not have any risk factors for coronary artery disease and 45% had only 1 risk factor. A history of previous myocardial infarction or coronary bypass surgery was present in 48 (67%) patients. In most patients (72%), angioplasty was performed during an admission for unstable angina or acute myocardial infarction. Single-vessel disease was present in 22% of patients. Successful angioplasty was performed in 92% of patients and major complications occurred in 8% of patients. Four patients (6%) died; in all of them, angioplasty was performed emergently to treat cardiogenic shock. None of 68 patients who underwent elective angioplasty for stable angina or a semielective procedure for unstable angina died during the hospitalization. We conclude that angioplasty can be performed safely in the carefully selected octogenarian. There is a low-risk subgroup of patients with limited disease in whom angioplasty is an attractive treatment strategy.

Myocardial damage in acute myocardial infarction is a time-dependent process. We examined the influence of very early thrombolytic therapy, comparing prehospital to hospital administration, in a consecutive group of patients with myocardial infarction on mortality, complications and the preservation of left ventricular function. Seven hundred sixty patients received early thrombolytic therapy: 114 at home (time delay to treatment 1.4 +/- 0.8 h) and 646 in hospital (2.1 +/- 1.0 h). Sixteen patients died in hospital and significant hemorrhage occurred in 15 (including three patients with hemorrhagic stroke). There was no difference between groups in hospital mortality or rate of complications. The duration of ischemia was shorter in patients with prehospital therapy (pain duration: 3.3 +/- 2.1 vs. 4.0 +/- 2.2; P0.05, and time to recovery of the ST segment in the electrocardiogram: 4.3 +/- 3.3 vs. 6.6 +/- 6.3; P0.002). Peak plasma creatine kinase was earlier in patients with prehospital therapy (11.2 +/- 5.0 vs. 13.0 +/- 5.8; P0.002), although there was no difference between groups in the absolute peak plasma level. Left ventricular function was assessed by contrast ventriculography 1 week after admission (616 patients). Ventricular function was better in patients with prehospital therapy: (ejection fraction of 58 +/- 13% vs. 54 +/- 15%; P0.05 and a left ventricular dysfunction index of 534 +/- 515 vs. 691 +/- 519 units; P0.05). We conclude that prehospital thrombolytic therapy is feasible and safe. Reperfusion is achieved earlier and more myocardium can be salvaged using this strategy without increasing the rate of complications.

The transradial approach has currently been advocated as an alternative catheferization method for coronary angiography and angioplasty, due to the recent miniaturization of angioplasty equipment. The purpose of this study was to assess the practical clinical applicability of this method. From June to November 1994, 100 patients underwent coronary angiography and angioplasty with the transradial approach. Their mean age was 66.6 ± 11.2 years, and 79 were men. In 4, radial puncture was not successful, and in 3, femoral access was necessary to complete the procedure. Coronary angioplasty was performed in 63 patients (76 lesions) with angiographic success (per lesion) of 96%. In 5 patients, a stent was successfully implanted. All patients were ambulatory on the day after the angioplasty procedure. In 98% of the patients, the introducer was taken out 1 to 4 hours after the procedure by local compression using a special custom-made device. No patient required blood transfusion. Major complications occurred in 2 patients; both had a cerebrovascular accident (1 probably not procedure-related), and both recovered. A radial pulse was palpated in 91 of the patients before discharge, and in 6 others, adequate flow could be heard with Doppler. In 2 patients, radial flow was restored within several weeks. None of the patients suffered from ischemia of the hand. Two patients had a small pseudoaneurysm successfully treated by local compression. Thus, coronary angioplasty can be performed safely using the transradial approach with relatively few vascular complications and with better patient comfort. However, the procedure is more time-consuming initially compared with the transfemoral approach due to a learning curve regarding equipment selection and catheter manipulation.

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 Hotter monitoring for perioperative myocardial ischaemia (defined as down sloping or horizontal ST-segment depression of ≥ 1mm) 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 STdepression. 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. However, only the cumulative ischaemia duration in the postoperative period remained associated with adverse cardiac outcome when subjected to multivariate logistic regression analysis ( p

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.

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)

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. There was little or no inhibition of vasorelaxation to nitroglycerin, isoproterenol, or 8-bromocyclic guanosine monophosphate by sickle erythrocytes or ghosts, demonstrating that sickle erythrocytes predominantly inhibit endothelium-dependent vasorelaxation. In addition, superoxide dismutase significantly diminished the inhibition of endothelium-dependent vasorelaxation as a result of sickle erythrocytes and ghosts. These findings indicate that sickle erythrocytes and their membranes interfere with endothelium-dependent vasorelaxation by inhibiting EDRF. Disruption of endothelial regulation of vasoreactivity may contribute to the development of vaso-occlusive phenomena in patients with sickle cell anemia.

Atheromatous coronary artery disease progresses by atheroma accretion, plaque rupture and thrombus formation, with or without spontaneous fibrinolysis [1–3]. The natural history may be altered by modifying risk factors in an attempt to induce regression [4], 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 [5, 6].

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.

Thalassemia patients succumb at a young age to congestive heart failure. Hitherto, attention has been focused on left ventricular function. This report emphasizes right ventricular dysfunction and abnormal pulmonary function. We performed cardiopulmonary evaluation, including echo-Doppler, spirometry, CO diffusion (Dco), and blood gas analyses in 35 patients with homozygous beta-thalassemia maintained by multiple blood transfusions. Six autopsy lung specimens were studied. Thalassemia patients exhibited pulmonary dysfunction, characterized by hypoxemia (85 percent of the patients were outside the 95 percent confidence limits), reduced lung volumes (51 percent), flow rates (63 percent) and Dco (50 percent). Right ventricular dysfunction was more prevalent than left ventricular dysfunction. Furthermore, 75 percent of the patients had evidence of pulmonary hypertension consistent with more frequent right ventricular rather than left ventricular dysfunction. Our findings suggest that in thalassemia patients, complex cardiopulmonary abnormalities precede the final outcome of congestive heart failure.

Objectives The study determines whether treatment of coronary disease by percutaneous coronary intervention (PCI) in the presence of severe aortic stenosis (AS) is feasible and defines which patients might benefit most. Background Severe symptomatic AS is considered a class I indication for aortic valve replacement (AVR). Many patients with AS have concomitant coronary artery disease (CAD), and the true reason for symptoms is often unclear. It is common practice to combine AVR with coronary artery bypass grafting. However, in some cases PCI alone might improve symptoms and allow surgery to be deferred. Methods We analyzed 38 consecutive patients who underwent PCI for CAD in the presence of significant AS between 1989 and 2004. Data included demographic factors, clinical features, angiographic, and echocardiographic information. Events during follow-up included PCI complications, improvement post-PCI, AVR, and death. Statistical analysis was used to assess the impact of PCI on outcome and survival. Results The mean age of the study group was 71 ± 9.3 years, and the mean aortic valve area was 0.84 ± 0.28 (0.4–1.2) cm 2 . Reasons for choosing PCI over surgery were patients' preference, high surgical risk, and cardiologist recommendation. Thirty-five patients (92.1%) reported symptomatic improvement after PCI, and no major PCI-related complications were recorded. Significant predictors for long-term event-free survival were good functional class ( P = .006) and single-vessel coronary disease ( P = .017). Conclusion PCI in patients with severe AS and significant CAD is safe, offers relief of symptoms in most cases, and has good long-term outcome in a subset of patients who have mild CAD and good functional class. This therapeutic approach should be considered in such patients and in those with high surgical risk.

C oronary stents were introduced in an attempt to overcome 2 main limitations of balloon angioplasty: acute occlusion and restenosis. Numerous reports showed that different stent designs are useful.1-3 The main problem of currently available metallic stents is the tendency for thrombotic occlusion. This is a serious complication that can cause acute myocardial infarction and death.4 Chronic anticoagulation decreases the occlusion rate but causes complications at the puncture site and increases the length of hospitalization and cost of the procedure.5 Recent abstracts have suggested that anticoagulation might not be necessary when stents are deployed with high-pressure balloon inflation with or without intravascular ultrasound proof of optimal deployment.6,7 This report will describe our initial experience with PalmazSchatz stents with emphasis on the risk of thrombotic occlusion. . . . Coronary stents were successfully deployed in 50 of 52 patients (96%). In the 2 patients in whom the stent was not deployed, the procedure was successfully completed with balloon dilatation. The mean age was 60 + 11 years, most patients (45) were men, and the indication for cardiac catheterization was stable angina in 29 and unstable or postmyocardial infarction angina in 21 patients. Twenty-seven stents were implanted to overcome acute closure or severe dissection that would have otherwise required emergency bypass surgery, 14 were implanted in lesions with previous restenosis, and in 11 patients stents were implanted electively as the initial therapy (mainly in saphenous vein grafts). Thirty-nine stents were implanted in native coronary vessels and 13 in saphenous vein grafts. Stents were deployed after target lesion predilatation using a balloon that matched the size of the normal artery. Stents were manually crimped on a balloon (usually 0.5 mm larger than the original balloon) and were deployed using 30-second inflation to 6 to 8 atm. Patients were treated with intravenous dextran for 24 hours and a combination of aspirin and dipyridamole. Treatment with warfarin was begun on the day of the procedure and was continued for 3 months, with a target international normalized ratio of 3 to 4. Heparin infusion was maintained with a target partial thromboplastin time of 80 to 100 seconds for >5 days, and for 1 day after target prothrombin level was achieved. Sheaths were removed from the femoral artery the morning after the

Prehospital thrombolysis preserves LV function, but its impact on long-term outcome has not yet been reported. We followed for 2–7 years, 362 patients (pts) who received IV thrombolysis since prehospital strategy was started in Jerusalem. CHF as judged by clinical symptoms and exercise performance were compared between 68 pts who received prehospital streptokinase, at 1.2 ± 0.6 hours of chest pain onset (group I) and 294 pts with in-hospital lysis after 2.2 ± 1.0 hours (group II). The difference in LV function measured at 1 week contrast ventriculography was small — Group 1 — EF 58 ± 15% vs Group II — 55 ± 14%, but a striking and significant change was observed in CHF disability (NYHA Grade II—IV) prevalence at follow-up. Disability 1Day 2Wks 3 Mos 1 Yr 2 Yr 3 Yr 6 Yr Gr I%pts Grll %pts 15] 25] * 2] 15] * 4] 20] * 9] 27] * 10] 27] * 11] 28] * 21] 34] * * P l 0.05 Similar significant changes between the two groups were observed for other complaints: pulmonary edema, orthopnea, paroxysmal nocturnal dyspnea, nocturia, peripheral edema, fatigue and angina pectoris. Thus, time gain through prehospital lysis prevents CHF symptoms and long-term disability and justifies more extensive use of early thrombolysis.

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, p0.001). 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.

Thirty-four patients with acute myocardial infarction were treated prospectively using a new strategy of prehospital intravenous streptokinase given by a physician-operated mobile intensive care unit. The 29 prehospital-treated patients who had experienced no previous myocardial infarction were compared to a similar group treated with streptokinase inhospital. Patients receiving streptokinase in the prehospital phase of acute myocardial infarction had smaller infarcts and better residual myocardial function than the group given streptokinase inhospital in terms of peak creatinine phospholdnase, ejection fraction, computer-derived dysfunction index, and electrocardiographic QRS score. The only difference between these groups at baseline was the duration of pain prior to initiation of streptokinase therapy. There were no major complications related to prehospital administration of streptokinase.

The pattern of contraction of the endocardial wall of the left ventricle in the right anterior oblique cineangiogram was studied by using a frame by frame radial technique and a fixed centroid without correction for rotation and translation motion during the cardiac cycle. Spatial defects of contraction were quantitated by measuring the shortening fraction of each radius and temporospatial defects by using a time-contraction integral. Twelve normal subjects were used as a basis for comparison. Thirty-two patients with isolated disease of the left anterior descending (LAD) coronary artery were divided into seven arbitrary clinicopathological subsets. Five subsets showed significant quantitative differences in contraction from the normal subjects but there was no significant difference between the subsets. They had a typical defect of contraction in the distal two thirds of the anterior wall, the apex and distal quarter of the inferior wall of the left ventricle. The subsets included: (1) patients who had undergone an anterior myocardial infarction and who had total occlusion of the LAD artery and a large anterior infarction on ECG; (2) patients with a previous classical myocardial infarction but with only 95% residual narrowing of the LAD; (3) patients with an anterior infarction and total occlusion of the LAD with return of the R waves in the anterior precordial leads; (4) patients with anterior infarction, LAD obstruction and left bundle branch block and (5) patients with anterior infarction but with early successful reperfusion with intracoronary streptokinase. Two other subsets, (1) patients with total obstruction of the LAD without a clinical myocardial infarction or (2) subtotal occlusion of the LAD without infarction, had mild left ventricular dysfunction at rest and did not differ significantly from normal.

Temporal changes in residual stenosis in the infarct-related coronary artery and ventricular function were studied in 30 consecutive patients with an acute myocardial infarction who received rapid, high dose intravenous infusions of streptokinase within 4 h of pain onset. Patients were studied 6 days and 3.9 +/- 1.3 months after the acute episode. Inferior infarction, early thrombolysis (less than 1.5 h after pain onset) and adequate reperfusion (less than 75% residual stenosis in the infarct-related coronary artery) were associated with smaller left ventricular infarcts, smaller ventricular volumes and better ventricular function. Residual stenosis tended to increase with time and in 6 patients the artery closed completely (1 with an overt clinical episode). Ventricular function and volumes improved progressively in patients with good initial function and less residual stenosis in the infarct-related coronary artery.

Purpose: To investigate the associations between specific preoperative 12-lead electrocardiogram (ECG) abnormalities, perioperative ischemia, and postoperative myocardial infarction or cardiac death in major vascular surgery. Methods: Two prospective studies on perioperative myocardial ischemia performed in two tertiary university hospitals were combined to include 405 patients. All preoperative ECGs were analyzed according to the Sokolow-Lyon criteria for left ventricular hypertrophy by investigators who were blinded to the patients' perioperative clinical course. Perioperative myocardial ischemia was detected by continuous ECG recording, and postoperative cardiac complications included myocardial infarction and cardiac death. Results: A total of 19 postoperative cardiac complications occurred (two cardiac deaths and 17 myocardial infarctions). Voltage criteria for left ventricular hypertrophy (78 patients, 19%) and ST segment depression greater than 0.5 mm (98 patients, 24.2%) on preoperative ECGs were both significantly associated with postoperative myocardial infarction or cardiac death (odds ratio, 4.2 and 4.7; p = 0.001 and 0.0005, respectively) and with longer intraoperative and postoperative myocardial ischemia. In each of the two study groups, a preoperative ECG abnormality that involved voltage criteria, ST segment depression, or both (134 patients, 33.1%) was more predictive of postoperative cardiac complications than any other preoperative clinical variable, including a history of myocardial infarction or angina pectoris, diabetes mellitus, pathologic Q-wave by ECG, or preoperative myocardial ischemia. The combined duration of intraoperative and postoperative ischemia and the preoperative ECG with either voltage criteria or ST segment depression were the only independent factors associated with adverse cardiac events by multivariate analysis ( p ≤ 0.0001 and p = 0.02, respectively). Conclusion: Left ventricular hypertrophy and ST segment depression on preoperative 12-lead ECGs are important markers of increased risk for myocardial infarction or cardiac death after major vascular surgery. (J Vasc Surg 1997;26:570-8.)

We evaluated the effectiveness of early intravenous administration of 750,000 units of streptokinase in 53 patients with acute myocardial ischemia treated by a mobile-care unit at home (9 patients) or in the hospital (44 patients). Treatment was begun an average (+/- S.D.) of 1.7 +/- 0.8 hours from the onset of pain. Non-Q-wave infarctions developed subsequently in eight patients, whereas all the others had typical Q-wave infarct patterns. In 81 per cent of the patients the infarct-related artery was patent at angiography performed four to nine days after admission. Vessel patency was independent of the time of treatment, but residual left ventricular function was time dependent. Patients treated less than 1.5 hours after the onset of pain had a significantly higher ejection fraction (56 +/- 15 vs. 47 +/- 14 per cent; P less than 0.05) and infarct-related regional ejection fraction (51 +/- 19 vs. 34 +/- 20 per cent; P less than 0.01) and a lower QRS score (5.6 +/- 4.9 vs. 8.6 +/- 5.5; P less than 0.01) than patients receiving treatment between 1.5 and 4 hours after the onset of pain. Patients treated earlier by the mobile-care unit also had better-preserved left ventricular function than patients treated in the hospital. We conclude that thrombolytic therapy with streptokinase is most effective if given within the first 1.5 hours after the onset of symptoms of acute myocardial infarction.

We studied six patients who suffered from angina pectoris but had angiographically patent major coronary arteries. Two of the patients suffered also from congestive heart failure. Three patients had supraventricular tachyarrhythmias. Three patients had conduction disturbances. During coronary angiography the patients had significantly reduced flow velocity of angiographic contrast medium compared with that in a control group. Echocardiographic and Doppler flow studies showed a tendency for symmetrical thickening of the left ventricular wall, enlargement of the right ventricle, and reduced compliance of both ventricles. Right ventricular endomyocardial biopsy revealed pathologic small coronary arteries with fibromuscular hyperplasia, hypertrophy of the media, myointimal proliferation, and endothelial degeneration. Capillaries had swollen endothelial cells encroaching on the lumen. Myocardial hypertrophy, lipofuscin deposition, and patchy fibrosis were also observed. These cases show that small-vessel coronary artery disease can cause classic angina pectoris. The diagnosis can be suspected when the coronary angiogram shows large patent arteries with slow flow of the angiographic contrast medium and it can be confirmed by endomyocardial biopsy.

Three-dimensional (3-D) images of the human left ventricle were reconstructed from 2-dimensional echocardiographic pictures. All images were recorded at held end-expiration from an optimal point where a high-quality parasternal long-axis view maximally visualizing the left ventricle could be obtained. Multiple short-axis views were obtained from the same reference point. Interactive computer techniques were used to reconstruct 3-D shells of endocardium and epicardium. End-diastolic and end-systolic outlines were superimposed after correcting for motion during the cardiac cycle to demonstrate wall motion. Images were displayed from different perspectives and regional wall thickness, thickening, and motion were then demonstrated using surface map displays. Volumes and derived indices of left ventricular function were calculated. The ejection fraction of normal patients was 69 ± 9%, compared to 57 ± 7% in infract patients; the latter results correlated well with contrast angiography. 3-D echocardiographic reconstruction provides the observer with a spatial appreciation of left ventricular wall motion and thickness, as well as useful quantitative information. The system requires only a standard echocardiographic recorder and simple computer hardware.

• Immune hemolytic anemia and chronic active hepatitis developed concurrently in a 76-year-old man after prolonged therapy with methyldopa. Both complications disappeared following cessation of treatment with the offending drug and a short course of a high-dose corticosteroid (prednisone). Inhibition of T-suppressor lymphocyte function by methyldopa may be instrumental in the emergence of autoimmune complications following usage of the drug. (Arch Intern Med1983;143:592-593)

A unique chemical intoxication by Dead Sea water and its resultant physiological effects of combined severe hypercalcemia and hypermagnesemia are described. Of 48 adult patients, 16 had at least one severe clinical manifestation of either disturbed sensorium or a syndrome similar to adult respiratory distress syndrome. The patients had tachyarrhythmias (11 of 38, 29%), conduction disturbance (nine of 37, 24%), and a normal QTc interval in the presence of severe hypercalcemia. Combined respiratory and metabolic acidosis and concomitant extreme hypercalcemia and hypermagnesemia, reaching serum levels up to 28.8 and 33 mg/dL, respectively, were responsible for most of the clinical findings. The adult mortality was 19%. Four pediatric patients with variable degrees of intoxication survived. Discriminant function analysis determined that admission serum calcium concentration of more than 15.5 mg/dL was the best predictor of mortality. In patients with severe intoxication, supportive medical treatment, including forced diuresis, was disappointing. Early dialysis for severe cases merits further study.

A patient in whom perforation of a percutaneously inserted intraaortic balloon resulted in a clot formation inside the balloon is described. The balloon could not be withdrawn percutaneously and was lodged in the femoral artery. It was removed surgically, and the artery was repaired.

Right ventricular infarction occurs in 19-43% of patients with acute inferior wall infarction (Lorell et al., 1979). Its clinical, hemodynamic, and anatomic features are well known and include associated inferior wall infarction, distended neck veins, clear lung fields, hypotension, and heart block (Cintron et al., 1981; Coma-Canella et al., 1979; Lloyd et al., 1981; Lopez-Sendon et al., 1981; Raabe and Chester, 1978; Rotman et al., 1974). Isolated right ventricular infarction is less frequent and occurs in 2.5-4.6% of autopsy studies of myocardial infarction (Cohn et al., 1974; Erhardt et al., 1976; Wartman and Hellerstein, 1948). This report describes a patient with isolated right ventricular infarction with unusual electrophysiological findings. Her initial electrocardiogram showed atrial escape rhythm with incomplete right bundle-branch block and left posterior hemiblock. Later, she developed atrioventricular (AV) block with supra- and infra-Hisian, "phase 4," conduction defects. The sinus malfunction and high degree AV block persisted over 2 weeks and an atrioventricular sequential pacemaker was implanted. Hymodynamic study showed that her cardiac output was highly dependent on the heart rate and properly timed AV interval, and the pacemaker was programmed accordingly.

Thirty-four patients with acute myocardial infarction were treated prospectively using a new strategy of pre-hospital intravenous streptokinase given by a physician-operated mobile intensive care unit. Prehospital treated patients who had experienced no previous myocardial infarction were compared to a similar group treated with streptokinase in-hospital. All patients underwent cardiac catheterization on day 6.Patients receiving streptokinase in the pre-hospital phase of acute myocardial infarction had smaller infarcts and better residual myocardial function than the group given streptokinase in-hospital in terms of peak creatine phosphokinase (900 v.1298 IU, p=0.023), ejection fraction (62 v. 55%, p=0,004), computer-derived dysfunction index (427 v. 727, p=0.003), and electrocardiographic QRS score (4.1 v. 6.4, p=0.001). The only difference between these groups at baseline was the duration of pain prior to initiation of streptokinase therapy (1.0 ± 0.4 hours vs. 1.9 ± 0.9 hours). There were no major complications related to pre-hospital administration of streptokinase.Pre-hospital stretokinase infusion is feasible, safe and practical. It reduces ischemia time because treatment is not delayed until hospital arrival and therapy limits infarct size. Thrombolytic therapy for acute myocardial infarction can be initiated at home and should not be limited to hospitalized patients.

Background Despite well-established medical recommendations, many cardiac patients do not exercise regularly either independently or through formal cardiac prevention and rehabilitation programs (CPRP). This non-adherence is even more pronounced among minority ethnic groups. Illness cognition (IC), i.e. the way people perceive the situation they encounter, has been recognized as a crucial determinant of health-promoting behavior. Few studies have applied a cognitive perspective to explain the disparity in exercising and CPRP attendance between cardiac patients from different ethnic backgrounds. Based on the Health Belief Model (HBM) and the Common Sense Model (CSM), the objective was to assess the association of IC with exercising and with participation in CPRP among Jewish/majority and Arab/minority patients hospitalized with acute coronary syndrome. Methods Patients (N = 420) were interviewed during hospitalization (January-2009 until August- 2010) about IC, with 6-month follow-up interviews about exercise habits and participation in CPRP. Determinants that predict active lifestyle and participation in CPRP were assessed using backward stepwise logistic regression. Results Perceived susceptibility to heart disease and sense and personal control were independently associated with exercising 6 months after the acute event (OR = 0.58, 95% CI: 0.42-0.80 and OR = 1.09, 95% CI: 1.02-1.17, per unit on a 5-point scale). Perceived benefits of regular exercise and a sense of personal control were independently associated with participation in CPRP (OR = 1.56, 95% CI: 1.12-2.16 and OR = 1.08, 95% CI: 1.01-1.15, per unit on a 5-point scale). None of the IC variables assessed could explain the large differences in health promoting behaviors between the majority and minority ethnic groups. Conclusions IC should be taken into account in future interventions to promote physical activity and participation in CPRP for both ethnic groups. Yet, because IC failed to explain the gap between Arab and Jewish patients in those behaviors, other explanatory pathways such as psychological state or cultural views should be considered as potential areas for further research.

• Fifty-one successive patients treated with intravenous streptokinase 1.7 ±0.8 (mean ± SD) hours after onset of symptoms of acute myocardial infarction were evaluated during a three-month posthospital follow-up period. Coronary angiography was performed four to nine days after the initial hospital admission. Twenty-eight patients had a second late angiogram. Forty-one patients had successful reperfusion but only 25% of all patients were without significant clinical cardiovascular manifestations during this period. Postmyocardial infarction angina pectoris occurred in 21 patients, an abnormal stress test result was present in 28 patients, eight patients developed congestive heart failure, and five patients had reinfarction. An intervention with percutaneous transluminal coronary angioplasty or coronary artery bypass graft was performed in 15 (37%) of 41 reperfused patients. A significantly higher intervention rate was present in patients treated with streptokinase within one hour following the onset of symptoms. Early reocclusion (within three months of the infarct) was noted in patients with 60% or more residual stenosis in their infarct-related coronary artery. These patients also had a significantly greater incidence of angina pectoris. Our findings indicate that early thrombolytic therapy of acute myocardial infarction preserves myocardium, and since the infarct-related artery is patent, but narrowed, the jeopardized area is responsible for a high-risk syndrome with an increased likelihood of ischemic symptoms. An early aggressive approach may be indicated, especially for patients with greater than 60% residual stenosis in their infarct-related coronary artery. ( Arch Intern Med 1987;147:237-240)

Background: In the HORIZONS AMI trial, bivalirudin monotherapy (Biv) compared to unfractionated heparin (UFH) plus gp IIb/IIIa inhibitors (GPI) resulted in reduced rates of major bleeding, decreased cardiac mortality and net adverse clinical events (NACE) in pts with STEMI undergoing primary PCI at 1 year. Whether the beneicial effects of Biv are independent of diabetic status and are sustained long term has not been reported.