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D D Waters

Publications and source records attributed to D D Waters.

At least 91 records · Page 5Linked to original sources
PubMed1986

Problems related to the detection of myocardial ischemia caused by coronary vasospasm.

We compared the sensitivity of three commonly used provocative tests, exercise, ergonovine and the cold pressor test, in a series of 34 hospitalized patients with well-documented, active variant angina. All tests were performed off medication at the same time of day, usually on 3 consecutive days. Angina was provoked by ergonovine in all 34 patients, by exercise in 17 and by the cold pressor test in only 5 (p less than 0.005). ST elevation developed during the ergonovine test in 32 (94%), during exercise in 10 (29%) and during the cold pressor test in only 3 (9%). With ergonovine one patient had ST depression only and one had no ECG changes. During the cold pressor test two patients had pseudonormalization of abnormally negative T waves and 29 had no ECG changes. Exercise induced T wave pseudonormalization in 4 patients, ST depression in 9 others and no ECG changes in 11. Thus, in patients with active variant angina, the sensitivity of the cold pressor test and exercise are too low to be useful clinically. Other studies suggest that the sensitivity of hyperventilation or provoked alkalosis is higher, but not as high as ergonovine administration. In patients who have become asymptomatic, either with treatment or spontaneously, the sensitivity of all tests decreases markedly. If such patients no longer have coronary spasm, the test is not a 'false negative' but a 'true negative'. Deaths have been reported following ergonovine administration and for this reason the test is not universally accepted.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Factors associated with progression of coronary artery disease in patients with normal or minimally narrowed coronary arteries.

This study was performed to identify the subset of patients with normal or with minimal (49% or less) stenosis of the coronary vessels who may be prone to progressive coronary artery disease (CAD). Data were collected from 51 patients (19 men, 32 women, mean age 48 years) with normal coronary arteries (20 patients) or with minimal narrowing (31 patients) on a first angiogram, who underwent repeat catheterization 4 to 120 months later (mean 52) because of persistent chest pain. Three classic lifestyle-related risk factors (systemic hypertension, cigarette smoking status and hypercholesterolemia) were noted; the number of diseased segments on the first angiogram was counted according to a 15-segment coding system. Progression of CAD required the consensus of 3 observers on a 30% or greater decrease in luminal diameter. Progression was recorded in 16 of 31 patients with minimal CAD and in 3 of 20 patients with normal coronary arteries (p less than 0.01). By multivariate logistic regression, progression was predicted by (1) number of diseased segments (p = 0.001), (2) age (p less than 0.01), (3) smoking status (p less than 0.05) and (4) initial cholesterol level (p less than 0.05). Using the probability computed by the logistic model, we could separate the 51 patients in groups with low (0 of 18), medium (9 of 23) and high (10 of 10) risk of progression. Thus, patients with normal or minimally narrowed coronary arteries at angiography form a heterogeneous population including both normal or borderline subjects and patients with CAD at its early stage. The latter condition was associated with presence of risk factors and to the angiographic extent of the disease.

Adult↗
PubMed1985

Percutaneous transluminal coronary angioplasty for the treatment of variant angina.

Among 268 patients undergoing percutaneous transluminal coronary angioplasty between February 1980 and January 1983, a total of 21 patients had variant angina, documented before angioplasty in 14 and after angioplasty in 7. Before angioplasty, all 21 patients had rest angina and 17 also had effort angina; single vessel coronary artery disease with 60 to 95% stenosis was present in all patients and the left anterior descending coronary artery was involved in all but 3 patients. Coronary angioplasty was successful in 19 patients (90%). Eight of the 19 patients remained symptom-free without coronary restenosis after successful angioplasty; in the other 11 patients, angina reappeared within 4 months, usually in association with restenosis. Of the nine patients with coronary restenosis, six had repeat angioplasty (five successful procedures and one failure), two received medical therapy and one underwent coronary bypass surgery. Patients in whom calcium channel antagonists were discontinued immediately after angioplasty had an exceedingly high coronary restenosis rate (8 [80%] of 10 successful attempts), but when calcium antagonists were continued for an average of 6 +/- 4 months after angioplasty, the restenosis rate was low (3 [21%] of 14 successful attempts). After a mean (+/- SD) follow-up period of 33 +/- 13 months, 1 patient had died and the 20 others (95%) were symptom-free; among these 20, 15 patients (75%) had been taking no antianginal drugs for more than 1 year, 2 still received calcium channel antagonists and 3 had had coronary bypass surgery. Repeat coronary arteriography performed 14 +/- 7 months after angioplasty in the 17 patients without angioplasty-related infarction or surgery showed 50% or less coronary stenosis in 13 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Comparison of clinical variables and variables derived from a limited predischarge exercise test as predictors of early and late mortality after myocardial infarction.

An exercise test limited to 5 METS or 70% of age-predicted maximal heart rate was performed 1 day before hospital discharge by 225 survivors of acute myocardial infarction, all of whom were subsequently followed up for at least 5 years. The mortality rate was 11.1% during the first year, but averaged only 2.9% per year from the second to fifth year. Over the entire follow-up period, the five variables that predicted mortality by multivariate analysis were QRS score, an exercise-induced ST segment shift, previous infarction, failure to achieve target heart rate or work load and ventricular arrhythmia during the exercise test. Because mortality differed markedly before and after 1 year, Cox regression analyses were performed separately for both of these periods. The factors that were predictive of mortality during the first year were an exercise-induced ST shift (p less than 0.0001, relative risk 7.8), failure to increase systolic blood pressure by 10 mm Hg or more during exercise (p = 0.0039, relative risk 4.3) and angina in hospital 48 hours or longer after admission (p = 0.0046, relative risk 3.4). None of these three variables was predictive of mortality after 1 year. Previous infarction (p = 0.0007), QRS score (p = 0.0042) and ventricular arrhythmia during the exercise test (p = 0.016) were predictive of mortality after the first year. Thus, clinical and exercise test variables are complementary predictors of mortality after myocardial infarction. An abnormal ST segment response during an early limited exercise test and angina in the hospital are common strong predictors of mortality to 1 year, but not thereafter. Late mortality correlates with markers of poor left ventricular function.

Adult↗
PubMed1985

Coronary angiographic significance of left anterior fascicular block during acute myocardial infarction.

The clinical and angiographic significance of isolated left anterior fascicular block occurring during the early stage of acute myocardial infarction was studied in 141 consecutive patients who underwent cardiac catheterization before hospital discharge. Left anterior fascicular block occurred in 15 of the 62 patients with an anterior wall infarction and in 13 of the 79 with an inferior infarction. None of the clinical characteristics differed among patients with or without left anterior fascicular block. The number of coronary vessels with significant stenosis, the Friesinger and the Gensini scores for severity of stenosis and the ejection fraction were also similar in the two groups. Patients with left anterior fascicular block had more severe narrowing of the coronary artery supplying the infarct zone (88 +/- 21 versus 70 +/- 35%, p less than 0.001) and tended to have less developed collateral circulation (collateral score 0.7 +/- 0.8 versus 1 +/- 0.8, p = 0.10). A significant stenosis of the left anterior descending coronary artery was found as frequently in patients with as in those without left anterior fascicular block (64 versus 65%); 29% of the patients with inferior wall infarction and left anterior fascicular block had left anterior descending coronary artery stenosis compared with 47% of the patients without this conduction disturbance (no significant difference). When the infarction was located anteriorly, a significant stenosis of the proximal segment of the left anterior descending coronary artery was present in 47% of the patients with and in 45% of the patients without left anterior fascicular block.(ABSTRACT TRUNCATED AT 250 WORDS)

Bundle-Branch Block↗
PubMed1985

A dose-ranging, placebo-controlled, double-blind trial of nisoldipine in effort angina: duration and extent of antianginal effects.

Maximal treadmill exercise testing at 1, 3 and 8 hours was used to assess the onset, duration and antianginal efficacy of the dihydropyridine slow channel calcium-blocking agent, nisoldipine, in an oral dose range of 5, 10 and 20 mg. A double-blind, randomized, placebo-controlled design was used involving 12 patients with stable effort angina. Exercise tolerance was significantly increased 3 hours after each dose, when the maximal beneficial effect occurred. The improvement was observed as early as 1 hour after the 10 and 20 mg dose, and persisted for 8 hours after the 20 mg dose. At 3 hours, the onset of an exercise-induced ST segment depression of 0.1 mV or greater was increased by 62 (p less than 0.05), 75 (p less than 0.01) and 117 seconds (p less than 0.01) with the 5, 10 and 20 mg dose of nisoldipine, respectively, compared with placebo. Similarly, time to onset of angina was significantly increased. The sum of exercise-induced ST segment depression at peak exercise was significantly decreased (p less than 0.05) from 8.7 +/- 2.3 to 6.7 +/- 1.8 and 6.4 +/- 2.0 mm, respectively, after the 10 and 20 mg dose of nisoldipine. The rate-pressure product was significantly greater with nisoldipine than with placebo at the onset of ischemia and at peak exercise (22.8 +/- 1.1 versus 20 +/- 1.4 X 10(3) U for the 20 mg dose; p less than 0.01). Thus, nisoldipine is an effective antianginal agent with a rapid onset of action that improves exercise tolerance, increases angina threshold and persists for at least 8 hours after oral dosing.

Aged↗
PubMed1985

Serial exercise testing in patients with effort angina: variable tolerance, fixed threshold.

To investigate the frequency and mechanism of variable threshold angina, seven treadmill exercise tests were performed in each of 28 patients with stable effort angina and exercise-induced ST segment depression. Each patient had tests at 8 AM on 4 days within a 2 week period and on 1 of these days had three additional tests at 9 AM, 11 AM and 4 PM. Time to 1 mm ST depression increased from 277 +/- 172 seconds on day 1 to 319 +/- 186 seconds on day 2, 352 +/- 213 seconds on day 3 and 356 +/- 207 seconds on day 4 (p less than 0.05). Rate-pressure product at 1 mm ST depression remained constant. Similarly, time to 1 mm ST depression increased from 333 +/- 197 seconds at 8 AM to 371 +/- 201 seconds at 9 AM and to 401 +/- 207 seconds at 11 AM and decreased to 371 +/- 189 seconds at 4 PM (p less than 0.01). Again, rate-pressure product at 1 mm ST depression remained constant. The standard deviation for time to 1 mm ST depression, calculated as a percent of the mean for each patient's seven tests and then averaged for the entire group, was 22 +/- 11%. The standard deviation for rate-pressure product at 1 mm ST depression, calculated in the same way, was significantly less at 8.4 +/- 2.8% (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

A randomized study comparing propranolol and diltiazem in the treatment of unstable angina.

One hundred consecutive patients hospitalized in the coronary care unit for unstable angina, excluding patients with Prinzmetal's variant angina, were randomized within 24 hours of admission to treatment with diltiazem (50 patients) or propranolol (50 patients). Also excluded were patients with previous coronary artery bypass surgery and those receiving a beta-receptor blocking agent at the time of hospital admission. Left ventricular function and the extent of coronary artery disease were similar in the two groups. During the hospital stay, the number of chest pain episodes decreased from a mean (+/- SD) of 0.75 +/- 0.1 per patient per day to 0.26 +/- 0.07 (p less than 0.05) with diltiazem and 0.29 +/- 0.1 (p less than 0.05) with propranolol therapy. The circadian distribution of chest pain episodes was affected similarly. After 1 month, 14 of the patients treated with diltiazem were symptom-free compared with 13 treated with propranolol. At a mean follow-up time of 5.1 months (range 1 to 15), death had occurred in two patients in each group and myocardial infarction in five diltiazem- and four propranolol-treated patients (difference not significant). Coronary artery bypass surgery had been performed in 21 diltiazem- and 19 propranolol-treated patients (difference not significant). Only 15 patients were symptom-free, 9 treated with diltiazem and 6 with propranolol. This similar result observed with the two forms of treatment suggests that coronary artery spasm may not be the main factor involved in unstable angina when Prinzmetal's variant angina is excluded. It also suggests that diltiazem can be used as an alternative to the usual treatment with beta-receptor blocking drugs.

Aged↗
PubMed1985

Angiographic findings after myocardial infarction in patients with previous bypass surgery: explanations for smaller infarcts in this group compared with control patients.

The incidence of previous coronary artery bypass surgery (CABS) in patients with acute myocardial infarction admitted to our hospital has risen from 2.3% to 11.2% in 6 years. We compared infarct size and the angiographically determined cause of infarction in 52 control patients and in 52 consecutive patients with acute myocardial infarction at least 2 months after they had undergone CABS. Baseline characteristics were similar in both groups except for a higher incidence of preexisting Q waves in the post-CABS group (22 vs 10; p less than .05). Indexes of myocardial infarct size were smaller in the post-CABS group compared with those in control patients: peak creatine kinease (CK) level (IU/liter) 1113 +/- 1094 (mean +/- SD) vs 1824 +/- 1932 (p less than .01), peak CK-MB level (IU/liter) 173 +/- 230 vs 272 +/- 332 (p less than .02), peak summed ST segment elevation (mm) 3.5 +/- 4.8 vs 8.2 +/- 9.9 (p less than .005), and QRS score on days 7 to 10, 1.9 +/- 3.0 vs 4.3 +/- 3.4 (p less than .001). Postinfarction left ventricular ejection fraction was higher in the post-CABS group (53 +/- 13%) compared with that in control patients (47 +/- 12%; p less than .05). The incidence of total occlusion of the artery to the infarct zone was similar in the post-CABS and control patients (33 vs 27), as was the incidence of one-, two-, and three-vessel disease (artery plus graft). Collateral blood flow to the infarct zone was found in 27 post-CABS patients and in 23 control patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1985

Programmed ventricular stimulation in survivors of an acute myocardial infarction.

The prognostic significance of programmed ventricular stimulation and its usefulness in relation to other forms of invasive and noninvasive testing was evaluated in 150 survivors of acute myocardial infarction. Ventricular tachyarrhythmias of 6 beats or more were induced in 35 (23%) patients. No significant differences existed between patients with inducible ventricular tachyarrhythmias and those without inducible ventricular tachycardia with respect to occurrence of spontaneous ventricular arrhythmias in the acute and early recovery phase of infarction or predischarge exercise-induced ischemia or arrhythmias, severity of coronary artery disease, or degree of left ventricular dysfunction. A higher incidence of inferior myocardial infarction was observed in patients with inducible ventricular tachycardia when compared with those without inducible ventricular tachycardia (66% vs 41%, p less than .01). During a mean follow-up of 10 +/- 5 months (range 2 to 19), there were two sudden deaths, three nonsudden deaths, and two additional patients developed sustained ventricular tachyarrhythmias. There was no significant difference between patients with and those without inducible ventricular tachyarrhythmias with respect to the occurrence of these events. In this study population, a lower mean ejection fraction (p less than .01), the presence of a ventricular aneurysm (p less than .05), and exercise-induced ventricular premature contractions (p less than .05) were predictors of sudden death and of spontaneous ventricular tachycardia. Thus, the findings of this study do not support the hypothesis that the induction of ventricular tachyarrhythmias in patients recovering from acute myocardial infarction identifies a group at high risk for sudden cardiac death.

Acute Disease↗
PubMed1984

Circadian variation in variant angina.

Thirteen hospitalized patients with variant angina were studied to assess circadian variation in disease activity. Over 48 hours, all angina attacks were noted, a continuous Holter electrocardiogram was recorded and 2 ergonovine tests were performed 12 hours apart, 1 at 4 AM and the other at 4 PM. Only 2 patients gave a clearcut history of more frequent nocturnal or early morning attacks. During the study period, 1.8 +/- 1.6 AM and 0.62 +/- 1.2 PM angina episodes per patient were reported (p less than 0.02), but a circadian pattern was apparent in only 4 patients. However, Holter analysis revealed 5.3 +/- 13.8 AM and 2.6 +/- 8.5 PM episodes of ST elevation per patient (p less than 0.05) and 8.1 +/- 13.9 AM and 3.2 +/- 8.5 PM episodes of ST elevation, ST depression or T-wave pseudonormalization (p less than 0.01). Ten of 11 patients with Holter abnormalities had more frequent AM than PM attacks (p less than 0.01). ST elevation developed during all 13 of the 4-AM and 12 of 13 of the 4-PM ergonovine tests. In 10 cases the ergonovine threshold at which the attack occurred was lower in the morning, in no case was it lower in the afternoon, and in 3 patients the morning and afternoon doses were identical (p less than 0.01). Thus, circadian variation in disease activity both for spontaneous and provoked attacks is present in most patients with variant angina, even though it is often not clinically apparent.

Adult↗
PubMed1984

Ventricular arrhythmias during ergonovine-induced episodes of variant angina.

Of 95 consecutive patients with active variant angina who underwent ergonovine testing in the coronary care unit while off treatment, 24 (25%) developed serious ventricular arrhythmias: ventricular tachycardia in eight, bigeminy in seven, pairs in five, and frequent ventricular extrasystoles in four. Ergonovine-induced arrhythmias were observed more often in patients with anterior than inferior ST segment elevation (p less than 0.05). ST segment elevation was significantly higher (10.3 +/- 8.1 vs 3.1 +/- 2.1 mm) in patients who developed arrhythmias. All ventricular arrhythmias began within 3 minutes after the onset of ST segment elevation. The intravenous administration of nitroglycerin eliminated arrhythmias in 22 of 24 cases; in only two patients did ventricular arrhythmias develop after the administration of nitroglycerin. Serious ventricular arrhythmias were found during spontaneous variant angina attacks in 14 of 24 patients with ergonovine-induced arrhythmias compared to 16 of 71 patients without ergonovine-induced arrhythmias (p less than 0.001). We conclude that arrhythmias during ergonovine testing are most often caused by ischemia and not reperfusion. Patients with arrhythmias during ergonovine-induced attacks are more likely to have arrhythmias during spontaneous attacks.

Adult↗
PubMed1984

Is progression of coronary artery disease occurring at bouts or as a continuous process? Serial cineangiographic studies in 44 patients.

In order to assess if coronary artery disease progression occurs as a slow, continuous process or at bouts, the coronary angiograms of 44 patients catheterized three times were reviewed. A previously developed logistic model, taking into account time interval between the angiograms, age, occurrence of unstable angina, and extent score of coronary artery disease, was used to compute a probability of progression from the second to the third angiogram. Two groups of patients were considered: those with (n = 15) and those without (n = 29) progression from the first to the second angiogram (PROGRESSION 1-2). A simulation provided in each group the distribution of the expected number of patients with progression from the second to the third catheterization. In the group without PROGRESSION 1-2, the observed number of progressions from the second to the third angiogram was in agreement with the expected one. However, in the group with PROGRESSION 1-2, the progression from the second to the third angiogram was more frequent than expected (p = 0.068). These results suggest that, in many patients, coronary artery disease progression is continuous over several years.

Cineangiography↗
PubMed1984

Clinical and angiographic factors associated with progression of coronary artery disease.

To characterize the clinical and angiographic factors associated with progression of coronary atherosclerosis, 313 consecutive medically treated patients who had had two coronary arteriograms 3 to 119 months (mean 39 +/- 25) apart were studied. One hundred eighty-one patients underwent recatheterization for stable angina, 52 for unstable angina and 80 for various other reasons. In addition to the conventional angiographic features present at the first angiographic study (number of diseased vessels 1.5 +/- 0.8, ejection fraction 59 +/- 11%), an extent score was defined based on the number of coronary segments with 5 to 75% narrowings from a 15 segment coding system. Multivariate logistic regression identified four independent predictors of progression of coronary artery disease: the interval between studies (p less than 0.0001), unstable angina (p less than 0.0001), a high extent score (p = 0.0001) and young age (p = 0.0026). In a subset of 74 patients aged 50 years or younger with, at the time of the first evaluation, an extent score of 4 or more, the probability of progression between 2 and 4 years and after 4 years was, respectively, 80 and 90% compared with 50% for the other patients. Risk stratification for progression of coronary artery disease can thus be obtained.

Adult↗
PubMed1984

Myocardial infarction in patients with previous coronary artery bypass surgery.

An increasing proportion of patients hospitalized with myocardial infarction have previously undergone coronary artery bypass surgery. To define this subgroup, 77 patients with acute infarction occurring 2 or more months (mean 52.8) after bypass surgery were compared with 77 control patients with infarction. Baseline characteristics of the groups were similar except that post-bypass patients were more often men (p = 0.02) and more likely to have had a previous infarction (37 versus 21, p = 0.008). Infarct size was smaller in the post-bypass group as assessed by peak creatine kinase (CK), peak CK-MB, maximal number of electrocardiographic leads with ST elevation, maximal summed ST elevation and QRS score measured 7 to 10 days after admission (p less than 0.001 for each variable). Five control patients but none of the post-bypass patients died in the hospital (p = 0.06). Serious complications (death, acute heart failure, ventricular fibrillation, second or third degree atrioventricular block) occurred in 24 control patients but in only 5 post-bypass patients (p less than 0.001). Angiography was performed after infarction in 45 of the 77 post-bypass patients. Occlusion of both a native coronary artery and its graft was found in 24 of the 45; these patients had had higher peak CK levels (p = 0.008) than the other 21 patients who had angiography. The probable causes of infarction in these 21 were disease progression in nonbypassed arteries or graft occlusion with arterial stenosis, or vice versa, and disease progression distal to a patent graft.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Exercise testing in the early period after myocardial infarction in the evaluation of prognosis.

Prognosis for the patient recovery from an acute myocardial infarction is related mainly to electrical instability, left ventricular function, residual ischemia, and extent of coronary atherosclerosis. Many procedures now exist that allow investigation of these various aspects of cardiovascular function and stratification of risk. No ideal marker of prognosis exists because prognosis is not related to a single factor, because the various determinants are often interdependent, and also because they are time dependent. Thus, the presence of ischemia may be particularly important in the first year when the risk is greater, whereas left ventricular function may be the most important factor thereafter. For this reason, an active strategy for detecting ischemia, by exercise testing or other means, may add to clinical observation. Exercise testing is a safe and noninvasive method that can provide information not only on residual ischemia but also on other aspects of cardiovascular function. Many parameters can be studied, such as ST segment elevation or depression, chest pain, ventricular arrhythmias, tolerance to exercise, completion or not of the test, and the heart rate and blood pressure responses. Some of these data are not specific and must be complemented by further investigation. Such as approach should allow an overall evaluation of the cardiovascular function of the patient and an assessment of risk, and help institute an optimal treatment.

Angina Pectoris↗
PubMed1983

Unstable angina and progression of coronary atherosclerosis.

We studied the progression of atherosclerotic coronary lesions in 38 patients who had previously undergone angiography and were later hospitalized for an episode of unstable angina pectoris, and in 38 matched patients with stable angina who had also undergone prior catheterization. Patients with unstable angina and those with stable angina were similar in terms of age (mean, 49 and 50 years, respectively), number of risk factors (1.5 per patient in both groups), interval between studies (mean +/- S.D., 44 +/- 31 and 35 +/- 31 months, respectively), number of diseased vessels on the first angiogram (1.52 in both groups), and initial ejection fraction (65 and 63 per cent, respectively). Progression of coronary lesions was demonstrated in 29 of the 38 patients with unstable angina, as compared with 12 of the 38 with stable angina (P less than 0.0005). Progression to 70 per cent or more stenosis was recorded in 21 of the patients with unstable angina but in only 5 of those with stable angina (P less than 0.0005). Also more frequent in the patients with unstable angina were multifocal progression (11 vs. 2, P less than 0.01) and progression of the left main or preseptal left anterior descending artery or both (9 vs. 1, P less than 0.01). Thus, we have demonstrated by angiography that unstable angina is associated with progression in the extent and severity of coronary atherosclerosis.

Adult↗