The influence of multiple clinical, angiographic and technical variables on the outcome of percutaneous transluminal coronary angioplasty was evaluated in a group of 76 consecutive patients with total coronary artery occlusion. Angioplasty was performed successfully in 53% of these patients. The likelihood of successful angioplasty was favorably influenced by: 1) a history of prior myocardial infarction in the distribution of the occluded arterial segment (p = 0.03); 2) an estimated maximal duration of arterial occlusion of less than 20 weeks (p less than 0.001); and 3) a length of nonvisualized arterial segment distal to the point of occlusion of less than 1.5 cm (p = 0.03). The outcome of coronary angioplasty was not significantly influenced by the vessel involved, the location of the occlusion within an involved vessel, the morphology of the occlusion (tapered versus abrupt) or the age and sex of the patient. There were no deaths and no vascular perforations. Four patients had recurrent coronary occlusion within 24 hours of the procedure; in three of these, recurrent occlusion was successfully treated with reangioplasty and in one, emergent surgical revascularization was performed. Embolic occlusion of an arterial branch distal to the point of total coronary occlusion occurred in 4 of the 40 successfully recanalized arteries. Seventy-five percent of patients having successful recanalization of an occluded coronary artery were free of the anginal symptoms that had prompted performance of the procedure at a mean follow-up period of 7.3 months. Thus, angioplasty of a total coronary artery occlusion can be performed safely and effectively, particularly in patients with a history of prior myocardial infarction, a brief estimated duration of coronary occlusion and a short nonvisualized occluded arterial segment.
A technique is described for angioplasty at coronary bifurcations. This simple approach utilizes a single guiding catheter, an exchange wire, and a conventional dilatation catheter and guidewire. With this "protective" guidewire technique, side branches at risk from occlusion during dilatation of a primary coronary segment can be protected and dilated secondarily; continual access to the threatened side branch is maintained with a "standby" exchange wire in the branch vessel.
Restenosis remains a limitation of directional coronary atherectomy. A subset of patients with larger vessels, shorter lesions or lesions treated with a larger (7F) device may have a more favorable outcome.
[3H]‐nitrendipine binding data and isolated tissue response for five calcium antagonists were evaluated in rabbit myocardium and aorta.
The [3H]‐nitrendipine binding site was qualitatively identical in myocardium and aorta, as the [3H]‐nitrendipine KD, KIs for nicardipine and nifedipine and interactions with verapamil, D600‐and diltiazem were not different in aortic and cardiac membranes prepared by similar means.
In contrast, the inhibition of the Ca2+‐induced contractile response in right ventricular myocardium and aortic ring segments indicated a > 10,000 fold selectivity of nicardipine for antagonism of vascular responses. This resulted in a different order of potency for calcium antagonist interaction with the [3H]‐nitrendipine binding site in cardiac membranes (nicardipine > nifedipine > D600 > verapamil > diltiazem) as compared to antagonism of myocardial tissue response (D600 > verapamil > nifedipine > nicardipine > diltiazem). In heart the difference between the potency of nicardipine in binding experiments and tissue response approached 4 orders of magnitude.
We conclude that tissue response selectivity of calcium antagonists is not explained by heterogeneity of [3H]‐nitrendipine binding sites.
In 43 patients with variant angina, the cardiovascular event rate during diltiazem therapy was compared with that in an equal time period before initiation of therapy. Cardiovascular events, that is, myocardial infarction, sudden death and hospitalization for prolonged angina, were decreased significantly (p less than 0.01) during the initial 6 months and mean 19.6 months of therapy. Based on the binomial principle, there were 22 events during the mean 19.6 months before therapy and 2 events during the equal time period on therapy. No patient died during follow-up. The frequency of angina was decreased by 94%. Diltiazem was well tolerated by all patients and no patient had to discontinue therapy because of adverse effects. It is concluded that long-term diltiazem therapy reduces cardiovascular events in patients with variant angina.
Diltiazem, a calcium channel blocking agent, has potent cardiovascular effects that are directly related to its influence on vascular smooth muscle, ventricular myocardium, and specialized conducting tissue. It causes coronary and peripheral vasodilation, has a negative chronotropic and dromotropic effect, and little to no negative inotropic effect in patients with normal ventricular function. Diltiazem has potential use in a wide variety of cardiovascular disorders. It has been shown extremely effective in relieving the coronary artery spasm associated with variant angina. When compared with nitrates in patients with exertional angina, diltiazem has similar efficacy. Preliminary work indicates it will have a therapeutic role in the treatment of unstable angina. Because of its ability to improve the balance between myocardial oxygen supply and demand and reduce cellular injury secondary to ischemia, it is likely that diltiazem will be of benefit in the treatment of acutely ischemic myocardium during cardiopulmonary bypass and possibly acute myocardial infarction. It has proven efficacy in treating re-entrant supraventricular tachycardia. Adverse effects are seen in less than 5% of patients, indicating that it is well tolerated.
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