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Biomedical subjects

D D Waters

Publications and source records attributed to D D Waters.

At least 73 records · Page 4Linked to original sources
PubMed1988

Restenosis and progression of coronary atherosclerosis after coronary angioplasty.

The relation between restenosis and progression of atherosclerosis in other coronary segments after angioplasty was studied in 98 consecutive patients with 110 coronary stenoses successfully treated with angioplasty. At early angiographic restudy (5 +/- 2 months after angioplasty) 37 patients (38%) had restenosis (defined as a stenosis greater than or equal to 50% of the luminal diameter or loss of greater than or equal to 50% of the gain achieved by angioplasty); progression of atherosclerosis was observed in 4 patients with and 7 without restenosis (13 versus 11%, p = NS). Ninety of the 98 patients underwent a late angiographic restudy a mean of 34 +/- 11 months after angioplasty. Late restenosis was found in one patient. Progression of coronary artery disease (defined as a greater than or equal to 20% decrease in the diameter of a vessel initially narrowed by greater than or equal to 50% or a greater than or equal to 30% decrease when the initial stenosis was less than 50%) was examined in relation to restenosis in 85 of the 90 patients. It occurred in 9 of 27 patients with and 22 of 58 patients without restenosis (33 versus 38%, p = NS). Restenosis developed more rapidly than did progression of disease. Diameter stenosis increased from 35 +/- 8 to 73 +/- 11% at the early restudy in lesions with restenosis; in lesions with disease progression it increased from 9 +/- 18 to 20 +/- 28% (p less than 0.001) at the early restudy to 53 +/- 21% (p less than 0.001) at the late restudy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Multiple coronary angioplasty: a model to discriminate systemic and procedural factors related to restenosis.

To assess the interrelation of clinical and procedural factors responsible for restenosis, 119 patients undergoing coronary arteriography were studied a mean of 5.8 +/- 3 months after successful multiple percutaneous transluminal coronary angioplasty. In all clinical, angiographic and procedural variables, the 119 patients undergoing repeat catheterization were similar to the 87 patients that did not. Overall, restenosis occurred in 74 (34%) of 215 lesions. Sixty-three patients had no restenosis, 44 had at least one restenosis and 12 had restenosis at all angioplasty sites. The statistical distribution of restenoses did not follow a binomial model, suggesting that restenosis is more than a lesion-specific phenomenon. Of all the clinical and procedural variables assessed by multivariate logistic regression analysis, only percent stenosis before angioplasty (p less than 0.01), diabetes mellitus (p less than 0.01) and percent stenosis after angioplasty (p less than 0.05) were predictive of restenosis in the entire group. Patients with no restenosis and patients with restenosis at all sites were not different with respect to procedural variables; however, patients with restenosis at all sites more often (p less than 0.05) had diabetes and recent onset angina. In contrast, patients with no restenosis differed from patients with isolated restenosis with respect to procedural variables: severity of stenosis before and after angioplasty, balloon/artery lumen ratio and maximal inflation pressure. Thus, procedural factors may be more related to isolated restenosis, but patient-related factors such as diabetes and recent onset angina may play a more important role in patients with multiple restenoses.

Aged↗
PubMed1988

Long-term prognosis after myocardial infarction in patients with previous coronary artery bypass surgery.

A group of 205 patients hospitalized with myocardial infarction 2 to 162 months (mean 66) after bypass surgery and 205 control patients with myocardial infarction were compared and followed up for 34 +/- 25 months after hospital discharge. At baseline the postbypass group contained more men (p less than 0.03) and more patients with previous myocardial infarction (p less than 0.06), but the groups were otherwise comparable. Indexes of infarct size were lower in postbypass patients: sum of ST elevation, QRS score, peak serum creatine kinase (CK) (1,115 +/- 994 versus 1,780 +/- 1,647 IU/liter) and peak MB CK (all p less than or equal to 0.001). Postmyocardial infarction ejection fraction was 45 +/- 15% in the postbypass group and 43 +/- 15% in the control group (p = NS); in-hospital mortality rate was 4 and 5%, respectively (p = NS). When patent grafts were taken into account, the two groups were comparable in extent of coronary artery disease. At 5 years after discharge, cumulative mortality was similar in the postbypass and control groups (30 versus 25%, respectively, p = NS). However, postbypass patients had more reinfarctions (40 versus 23%, p = 0.007), more admissions for unstable angina (23 versus 18%, p = 0.04) and more revascularization procedures (34 versus 20%, p = 0.04) than did control patients. The total for these events at 5 years was 70% in the postbypass group and 49% in the control group (p = 0.001). Thus, although patients with previous bypass surgery who develop acute myocardial infarction have a smaller infarct, their subsequent survival is no better than that of other patients with acute myocardial infarction. They experience more reinfarctions and unstable angina. Previous bypass surgery is an important clinical marker for recurrent cardiac events after myocardial infarction.

Angiography↗
PubMed1988

Regression of coronary atherosclerosis. Angiographic perspective.

The influence of dietary or pharmacological intervention on coronary atherosclerosis can best be assessed by performing serial coronary arteriography on patients at high risk for coronary disease progression who are randomised into controlled trials. Changes in coronary artery lesion diameter of less than 20% cannot be accurately assessed by visual interpretation, because of inter- and intra-observer variability. The introduction of quantitative, computer-assisted measurements of coronary lesions has reduced variability and greatly improved the precision of measurements. Both cholestyramine and colestipol-niacin have been shown to reduce the rate of progression of coronary atherosclerosis; however, in both studies coronary lesions were assessed visually and no quantitative measurements were reported. A marked reduction in serum cholesterol appears to be the intervention that is most likely to prevent the progression or induce regression of coronary atherosclerosis. Quantitative angiographic measurement techniques should be used in clinical trials designed to assess cholesterol-lowering interventions.

Angiocardiography↗
PubMed1988

Apical hypertrophic cardiomyopathy: clinical and angiographic characteristics of the first Canadian series.

Originally described in Japan, 'apical hypertrophic cardiomyopathy' has now been reported in many other countries. A series of eight patients who present with the classic 'spade-like' left ventricular angiographic pattern are reported; five of them also had hypertension. Thus, this angiographic pattern may not be specific for apical hypertrophic cardiomyopathy and may be seen in acquired heart disease.

Adult↗
PubMed1987

Early results, complications and restenosis rates after multilesion and multivessel percutaneous transluminal coronary angioplasty.

Initial results, complications, restenosis rates and clinical outcomes were compared in 78 patients undergoing multilesion and 128 patients undergoing multivessel percutaneous transluminal coronary angioplasty (PTCA). Multilesion PTCA was defined as a procedure in which a proximal PTCA site had to be crossed to dilate a distal severe narrowing and multivessel PTCA as multiple dilatations without having to cross 1 severe narrowing to dilate another. The clinical and angiographic features of the 2 groups were similar. More sites per patient were attempted among those who underwent multilesion PTCA. Primary success rate per lesion was 86% (236 of 274) among those who underwent multivessel and 73% (155 of 211) among those who underwent multilesion PTCA (p less than 0.001). A success rate of 81% (101 of 124) for proximal lesions among those with multilesion PTCA was not significantly worse than that for those with multivessel PTCA; however, lesions distal to proximal sites had a success rate of only 62% (54 of 87), worse than either those with proximal stenoses or multivessel PTCA (p less than 0.005). Arterial diameter, severity of stenosis or procedural variables did not account for this difference. Complication rates were similar in the 2 groups. Despite a poorer success rate among patients with multilesion PTCA, clinical improvement to functional class 0 or 1 occurred in more than 70% of patients in both groups and was equal in patients with and without successful distal dilatations. Restenosis rates per lesion in patients with multivessel (31%) and multilesion (30%) PTCA were similar.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Comparative antianginal effects of nisoldipine and nifedipine in patients with chronic stable angina.

The acute antianginal effects of 5 mg and 20 mg nisoldipine were compared with 20 mg nifedipine and placebo. Maximal treadmill exercise testing was performed before and 3 hours after drug administration in 10 patients with chronic stable angina. Resting heart rate and systolic blood pressure were unchanged following low-dose nisoldipine, but 20 mg nisoldipine and 20 mg nifedipine increased heart rate and decreased systolic arterial pressure (p less than 0.05). Time (in seconds) to the onset of 0.1 mV ST segment depression was significantly prolonged after 5 mg nisoldipine (+60 +/- 53; p less than 0.05) and 20 mg nisoldipine (+100 +/- 78; p less than 0.01) but not after 20 mg nifedipine (+48 +/- 131; p = NS). Total exercise duration increased significantly following 5 mg and 20 mg nisoldipine (p less than 0.01 and p less than 0.001, respectively) but only slightly following nifedipine (p = NS). The maximal rate-pressure product was increased to a similar degree following doses of both nisoldipine and nifedipine (p less than 0.05). Nisoldipine is an effective antianginal agent which performs well in comparison to nifedipine.

Aged↗
PubMed1987

Early postinfarction ischemia: clinical, angiographic, and prognostic significance.

Early ischemia, defined as angina with transient ST-T changes during hospitalization, 24 hr or more after an acute myocardial infarction (MI), was observed in 79 (18%) of a consecutive series of 449 patients surviving an MI and catheterized a mean of 10 +/- 3 days after admission. Three clinical factors present 24 hr after admission could identify patients at low, medium, and high risk of factors had a risk greater than 50% and the 118 patients with Q wave MI, no previous angina, and absence of risk factors had a risk of less than 8%. The angiographic correlates of early ischemia were number of vessels with 70% or more stenosis (2.1 +/- 0.8 vs 1.7 +/- 0.8/patient, p less than .0001), number of diseased coronary artery segments (2.8 +/- 1.4 vs 2.1 +/- 1.2, p less than .0001), left anterior descending coronary involvement (77% vs 62% of patients, p = .01), number of normally contractile segments at jeopardy because of a coronary stenosis (1.9 +/- 1.3 vs 1.3 +/- 1.1/patient, p less than .0002), collateral circulation at jeopardy (24% vs 15% of patients, p less than .005), and fewer collateral vessels distal to a tight stenosis (59 vs 72% of patients, p = .04). The stepwise logistic regression retained one angiographic and two clinical independent predictors of early ischemia: number of diseased vessels (p = .0008), presence of a non-Q wave MI (p = .0027), and previous angina (p = .017).(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Angiography↗
PubMed1987

Long-term prognosis of patients with variant angina.

The long-term prognosis of variant angina and the factors influencing it were assessed in 217 consecutive patients hospitalized in our coronary care unit and followed for a mean of 65 months (range 2 to 123). Cardiac death occurred in 30 patients and an additional 54 experienced a nonfatal myocardial infarction. Survival at 1 and 5 years was 95% and 89%, respectively; survival without infarction was 83% and 69%. Coronary disease and the degree of disease activity were strong predictors of survival by Cox analysis. Survival at 1 year was 99%, and that at 5 years was 95% and 94%, respectively, for patients with one-vessel disease (n = 81) and for those without stenoses of 70% or greater (n = 87). Survival at 1 and 5 years was only 87% and 77% for those with multivessel disease (n = 40). The Cox analysis selected left ventricular function, initial treatment, extent score, duration of angina at rest, and disease activity as multivariate predictors of survival without infarction. Coronary disease was a strong predictor (p less than .0001) of survival without infarction by univariate analysis. Treatment with nifedipine, diltiazem, or verapamil improved survival without infarction compared with other medical treatment (p = .002). Myocardial infarction occurred most commonly soon after diagnosis in patients with a short history of angina at rest. Late coronary events were almost never preceded by resting angina.

Adult↗
PubMed1987

'Second generation' dihydropyridine calcium antagonists. Greater vascular selectivity and some unique applications.

The newer dihydropyridine calcium antagonists are structurally related to nifedipine, but may provide greater vascular selectivity and wider clinical utility. Five new dihydropyridines-nisoldipine, nicardipine, nimodipine, felodipine and nitrendipine-are reviewed with regard to their preclinical pharmacology, haemodynamic effects and clinical indications. Nisoldipine is a potent arterial vasodilator with minimal electrophysiological and negative inotropic effects. Although data are still preliminary, the drug has shown some efficacy in both exertional angina and essential hypertension. The dosing interval is not yet clearly established, but may be twice daily. Utility in congestive heart failure awaits confirmation, but preliminary studies are promising. Nicardipine is an especially potent peripheral, cerebral and coronary arterial vasodilator that causes 10-fold less myocardial depression in animals than nifedipine, and may provide important cardioprotective effects during ischaemia. Human haemodynamic studies have confirmed nicardipine's lack of negative inotropism, its ability to reduce coronary and peripheral vascular resistance, and its lack of effect on cardiac conduction. Several controlled trials have documented its efficacy in exertional angina, vasospastic angina, and essential hypertension. Nicardipine's potential as an antiatherosclerotic agent is currently under investigation. Nimodipine is undergoing a unique clinical development programme aimed at cerebrovascular disorders. In almost all species, nimodipine selectively increases cerebral blood flow and reverses cerebral artery spasm without altering cerebral oxidative metabolism or systemic blood pressure. In humans, a large, double-blind, placebo-controlled trial in subarachnoid haemorrhage showed that nimodipine significantly reduced the severity of neurological deficits associated with delayed cerebral vasospasm. Several uncontrolled trials with larger numbers of patients support these results. Nimodipine has also proved useful in reducing cerebral artery spasm during intracranial surgery, and in the prophylactic treatment of migraine headaches. A preliminary study of nimodipine in acute stroke showed promising results in limiting neurological disability. Felodipine is a very potent systemic arterial vasodilator with negligible myocardial depressant activity. It is also a renal artery vasodilator. Unlike the other new dihydropyridines, felodipine prolongs the A-H interval on electrophysiological testing, but only to about 50% of that observed with verapamil. Felodipine is undergoing clinical trials in essential hypertension.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Previous coronary artery bypass grafting as an adverse prognostic factor in unstable angina pectoris.

Among 252 patients hospitalized for unstable angina in 1982 and 1983, 54 (21%) had undergone coronary artery bypass grafting (CABG) a mean of 55 months earlier (range 1 to 168) (CABG patients). This group was compared with a group of 54 randomly selected patients with unstable angina without previous CABG (control patients). The 2 groups did not differ with respect to clinical characteristics at admission or hospital course. Coronary arteriograms, recorded in all but 4 CABG patients, revealed multivessel stenoses of at least 70% luminal diameter in 40 CABG and 32 control patients (p less than 0.05), but when patent grafts were considered, the groups were comparable. Overall, 48 of 112 grafts were totally occluded and 14 had stenoses at least 70% in diameter. Complete or almost complete revascularization was feasible in 39 of 52 control and only 9 of 42 CABG patients (p less than 0.001). By 1 year, 46 control patients and 20 CABG patients had undergone CABG or coronary angioplasty (p less than 0.001); 42 of 53 control patients and only 22 of 50 CABG patients were in functional class 0 or I (p less than 0.001). Cumulative adverse events (5 deaths, 10 myocardial infarctions and 15 cases of recurrent unstable angina) were more frequent in the CABG group, 20 vs 10 (p less than 0.05). Thus, although their clinical features and hospital course are similar, patients with unstable angina who have undergone previous CABG do not do as well as other patients with unstable angina because they are less amenable to revascularization.

Angina Pectoris↗
PubMed1986

Long-term reproducibility and significance of provokable ventricular arrhythmias after myocardial infarction.

The long-term reproducibility and significance of inducible ventricular arrhythmias were assessed in 21 survivors of a myocardial infarction. Programmed ventricular stimulation performed a mean of 12 +/- 2 days (range 8 to 18) after infarction provoked ventricular fibrillation in 2 patients, sustained monomorphic ventricular tachycardia in 8 and nonsustained ventricular tachycardia in 11. Patients were restudied using the same protocol a mean of 8 +/- 2 months (range 4 to 11) after infarction. All patients underwent programmed ventricular stimulation studies in the absence of antiarrhythmic drug treatment. Ventricular tachyarrhythmias could be reinitiated in 16 patients (76%): ventricular fibrillation in 2, sustained ventricular tachycardia in 5 (monomorphic in 4) and nonsustained ventricular tachycardia in 9. A preponderance of inferior infarction was observed among patients with reinducible tachycardias (9 of 16 patients versus 0 of 5 with noninducible tachycardias) (p less than 0.05). No significant difference existed between patients with and without reinducible arrhythmias with respect to severity of coronary artery disease, degree of left ventricular dysfunction, occurrence of ventricular fibrillation in the acute phase of infarction and ventricular arrhythmias detected by 24 hour ambulatory electrocardiographic (Holter) monitoring. There was no significant difference between patients with and without a positive late study in stimulation thresholds, ventricular refractory periods, time interval between initial and repeat testing and use of beta-adrenergic blocking agents. During a mean follow-up period of 17 months (range 10 to 23) one patient with inducible sustained monomorphic ventricular tachycardia at both studies died suddenly. The remaining patients have survived follow-up without experiencing an arrhythmic event.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗