Hidemasa Kitazume

Clinical significance of isolated coronary bridges: Benign and frequent condition involving the left anterior descending artery

Review of 658 normal cineangiograms performed in the cardiac laboratory of the Cleveland Clinic during 1974 revealed myocardial bridging in 81 patients (12 % ). Maximal systolic compression was measured and compared to diastolic dimension above and below the obstruction by means of a programmable digital caliper. Systolic bridging involved the left anterior descending coronary artery in all cases and was mild in 26 patients, moderate in 55 patients, and severe in 11 patients. Seventy per cent of the patients were men and 30% were women. The majority had atypical symptoms although 15 patients were thought to have angina pectoris. Fiveyear survival rate was 97.5 % . No survivor had acute myocardial infarction during this follow-up period of 5 years. In the patient with normal coronary arteries and normal left ventricular function, myocardial bridging is benign. Myocardial bridging of coronary arteries was recognized and described by Black’ in 1796. If specifically sought at autopsy, such bridges are found in 5 % to 86% of hearts examined.2-4 These bridges also can be recognized arteriographically as a systolic compression of the vessel involved. A prevalence of 0.5% to 1.6% has been reported.5p6 It has been suggested that myocardial bridges, by reducing myocardial blood flow in systole, are responsible for cardiac ischemia,5*7 acute myocardial infarction (AMI),7-g ventricular fibrillation,‘O and sudden death.” Furthermore, it has been implied that myocardial bridging may have the same significant clinical morbidity and mortality as coronary atherosclerosis.12

Progression and regression of coronary atherosclerosis: Relation to risk factors

Epidemiologic studies have recognized the association of certain clinical characteristics, called “risk factors,” with the incidence and prevalence of coronary artery disease. l-lo Although association does not imply causation, an assumption of “probable cause” has been made by some2 and extraordinary efforts have been undertaken to favorably alter these factors in affected “high-risk” individuals and in society at large (primary prevention).” Similar measures have been recommended for patients with proved disease (secondary prevention).“. l2 In the patient with angiographically documented disease, death can be related to the number of coronary arteries involved, to the severity of involvement, and to left ventricular function.13-‘7 Risk factors are less clearly related to prognosis.‘“’ 14, l6 In the patient with disease, it can also be demonstrated that progression occurs in relation to time, increasing vessel involvement and left ventricular dysfunction.18,1g Risk factors at initial catheterization have not been found helpful in determining which cases will progress. 18-20 There has been little evidence to suggest that alteration of these risk factors in the individual who already has disease either retards or reverses the disease, thereby altering the risk of death.

Myocardial bridges in obstructive hypertrophic cardiomyopathy

It has been shown that in the patient with normal coronary arteries and normal left ventricular contractility, myocardial bridging does not reduce surviva1.l Hypertrophic cardiomyopathy, however, may alter its significance: Ishimori et al2 have shown the prevalence of angiographically recognized bridges to be higher in patients with left ventricular hypertrophy secondary to cardiomyopathy, aortic stenosis, and hypertension. Noble et al3 noted left ventricular hypertrophy or cardiomyopathy in 4 of 11 patients (36%) with systolic compression of 50% or more in the left anterior descending coronary artery. Two of the four patients with systolic compression of 75% or more and abnormal lactate extraction during atrial pacing had left ventricular hypertrophy. Also, one of three patients with myocardial bridging who suddenly died during exercise4 may have had hypertrophic cardiomyopathy. If hypertrophic cardiomyopathy alters the pathologic significance of myocardial bridging, long-term survival in these patients should be reduced when significant myocardial bridging is present.

Segmental analysis of the rate of progression in patients with progressive coronary atherosclerosis.

Bruschke et al.’ have shown that the likelihood of finding progressive coronary atherosclerosis at second catheterization increases in relation to time and severity of the initial lesion. Defining a rate of progression, however, has been difficult. Sudden, unpredicted events intermittently punctuate the clinical course of patients with coronary atherosclerosis, suggesting that there may be more than one rate of progression (fast versus slow), or that there may be some events occurring independently of time as a function of other variables.

Combined thrombolytic therapy and coronary angioplasty for acute myocardial infarction

From September, 1983, to August, 1984, combined thrombolytic therapy and percutaneous transluminal coronary angioplasty was used to treat 22 cases of acute myocardial infarction. Initial coronary angiograms showed total obstruction in 13 and severe stenosis in 9. Intracoronary infusion of urokinase reopened 7 of 13 totally occluded lesions but left a residual severe stenosis. Coronary angioplasty opened all of the remaining totally obstructed lesions and decreased the stenosis in 14 of 16 stenosed lesions. These procedures were performed 0.5 to 24 hours after the onset of chest pain. Lesions were not successfully dilated in two patients, because of arterial dissection in one and rethrombus formation in the other. One patient died from progressive hypotension beginning during the procedure, despite technically successful coronary angioplasty. Eighteen of the 20 successfully dilated lesions were patent at repeat angiography performed 1 to 3 weeks later. One successfully dilated lesion occluded 8 days after the procedure and was redilated by a larger sized balloon.

Repeat coronary angioplasty as the treatment of choice for restenosis

A prospective study was performed to determine whether multiple repeat coronary angioplasty can achieve final lesion patency after restenosis. Between 1983 and 1992, 1455 lesions (excluding acute myocardial infarction or total occlusion) were successfully dilated for the first time. Only 941 (68%) of the 1385 lesions followed up showed improved coronary flow (< or = 70% stenosis) after the first procedure. However, 1248 (93%) of 1345 lesions showed improved coronary flow after angioplasty had been repeated as many as three times, and 1268 (94%) of 1345 did so after as many as six procedures. Only 23 (1.6%) lesions required four or more procedures, and 20 of them showed final patency. These findings indicate that repeat angioplasty can be used as a reasonable treatment strategy for restenosis.

Magnum Meier wires with Crag Fx wire catheter for total occlusive coronary arteries

Magnum Meier wire was used with Crag Fx wire catheter instead of Magnum balloon catheter to facilitate wire crossing through total occlusion by improving flexibility of the system without losing wire pushability. Of 372 coronary angioplasty procedures performed between January 1994 and April 1995, there were 12 subacute occlusions with an interval of 3 wk or less and 30 chronic occlusions with an interval of > 3 wk. Regular over-the-wire-type balloon catheters failed to dilate four subacute occlusions and nine chronic total occlusions. Magnum Meier wire with Crag Fx wire catheter was tried for one subacute occlusion and four chronic occlusions that were undilatable with a regular balloon system and successfully dilated the subacute occlusion and three of the chronic occlusions. The lesions successfully dilated by this new approach were either long or tandem lesions in vessels that were excessively tortuous or showed an acute angle at the orifice. Thus the Magnum Meier wire with Crag Fx wire catheter can be a useful tool for dilating totally occluded lesions in tortuous coronary arteries.

Long-term angiographic prognosis of lesions dilated by coronary angioplasty

BACKGROUND To examine the long-term outcome of coronary angioplasty, lesions that remained patent after 3 to 12 months were monitored angiographically at 3-year intervals. There were 252 lesions successfully dilated (from 83% +/- 13% preprocedural stenosis to 19% +/- 14% residual stenosis) between 1983 and 1986 that remained patent on follow-up angiography (23% +/- 15% stenosis) and were monitored further at our outpatient department. METHODS AND RESULTS Repeat angiography was done for 186 lesions at 2 to 4 years and showed that 179 were patent (0% to 50% stenosis), one had mild stenosis (55% to 70% stenosis), and six had severe stenosis (75% to 100% stenosis). Angiography was repeated for 138 lesions at 5 to 7 years, showing that 127 were patent, four had mild stenosis, and seven had severe stenosis. Finally, angiography was performed for 78 lesions at 8 to 10 years, showing that 63 were patent, four had mild stenosis, and 11 had severe stenosis. CONCLUSIONS Although numerous lesions were lost to follow-up, most appeared to remain patent for 4 years, after which a significant number developed restenosis.

751-6 Multiple Repeat Coronary Angioplasty for Final Lesion Patency

To demonstrate that multiple repeat coronary angioplasty can be solely utilized to achieve final lesion patency after restenosis, such a protocol was prospectively applied for restenosis since 1983. Bypass surgery was only considered for 1) new left main trunk lesions, 2) symptomatic restenosis where angioplasty was either unsuccessful or unsuitable, and 3) patient preference. Between 1983 and 1992, 1455 lesions (acute myocardial infarction or total occlusion excluded) were successfully dilated for the first time. Although only 941 (68%) of the 1385 lesions studied showed satisfactory patency (≤ 70% stenosis) after the first procedure, 93% (1248/1345 studied) showed satisfactory patency after repeating angioplasty up to 3 times and 94% (1268/1354 studied) after repetition up to 6 times. Only 23 lesions 11.6%) required 4 or more procedures and 20 of them showed final patency. Disease aggravation (either impossible or failed repeat angioplasty, acute infarction, or sudden death) occurred in 43 lesions (3.2%). Bypass grafts were done for 11 lesions of 7 patients, mostly due to disease progression at the left main trunk. Dilatation (stenosis) Patent (0–50%) Mild (55-70%) Re-do(75%-) Grafts(75%-) Medical(75%-) Aggravated # Withdrawal Cumulative 0–70% No * 1st 874 67 384 9 16 32 73 941 1382 2nd 221 22 97 0 6 7 31 1184 1351 3rd 53 11 23 0 1 3 6 1248 1345 4th 11 1 8 1 0 1 0 1261 1345 5th 3 3 2 0 0 0 0 1267 1345 6th 1 0 0 1 0 0 0 1268 1345 * :1763- ∑ Withdrawal # :sudden death. acute infarction or irreversible occlusion Conclusion These findings indicate that 1) repeat angioplasty can be the main treatment strategy for restenosis, 2) multiple repeat angioplasties (up to 6 times) can be effective and rarely aggravate coronary anatomy and 3) disease aggravation must be prevented to improve the final patency rate of repeat ang ioplasty.

Progression of Coronary Atherosclerosis in Nonoperated Patients: Relation to Risk Factors

Important determinants of progression have recently been described by Bruschke and colleagues (1981). Careful analysis of sequential coronary cineangiograms obtained in 256 nonoperated patients with significant coronary atherosclerosis showed time to be the most important determinant of progression. In addition, the initial severity of disease could be correlated to progression, whereas risk factors at first study could not. If progressive coronary atherosclerosis occurs in relation to time and initial severity of disease independently of risk factors, “secondary prevention” by risk-factor modification may not be possible. We studied 302 patients to determine the relation of progression to risk factors.