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Biomedical subjects

D T Kelly

Publications and source records attributed to D T Kelly.

At least 73 records · Page 4Linked to original sources
PubMed1985

Left ventricular response to exercise in coronary artery disease: relation to myocardial ischaemia and effects of nifedipine.

To assess the relationship between left ventricular (LV) response to exercise and myocardial ischaemia, 40 patients with coronary artery disease (CAD) and 17 control subjects underwent radionuclide ventriculography at rest and during semiupright exercise. In 14 of the 40 patients with CAD, radionuclide exercise studies were repeated 20 min after 20 mg of sublingual nifedipine. Patients with CAD had increases in both LV end-diastolic and end-systolic volumes and no change in ejection fraction during exercise. End-systolic volume increased and ejection fraction decreased significantly more in patients with multivessel disease, exercise-induced angina and/or ischaemic ST segment depression. Nifedipine reduced angina and ST-segment depression during exercise, attenuated exercise-induced increase in end-diastolic and end-systolic volumes and improved ejection fraction. This study suggests that in patients with CAD, the response of LV volumes and ejection fraction to exercise is related to the degree of exercise-induced myocardial ischaemia and nifedipine improves exercise LV performance.

Adult↗
PubMed1985

Evaluation of relationship between myocardial contractile state and left ventricular function in patients with aortic regurgitation.

We studied the relationship between myocardial contractile state and left ventricular functional response to exercise in 14 asymptomatic patients with isolated moderate-to-severe aortic regurgitation and six control subjects. The slope of the systolic blood pressure-left ventricular end-systolic volume (pressure-volume) relationship determined by radionuclide ventriculography during angiotensin infusion was used as an indirect measure of myocardial contractility and was compared with left ventricular ejection fraction at rest and during both isometric handgrip and dynamic bicycle exercise. The slope of the pressure-volume relationship was significantly lower in patients with aortic regurgitation than in the control subjects (1.75 +/- 0.57 vs 2.78 +/- 0.42, p less than 0.01). The slope correlated exponentially with resting ejection fraction and was linearly related to changes in left ventricular ejection fraction during both handgrip and bicycle exercise. In patients with aortic regurgitation, resting ejection fraction may overestimate myocardial function. The slope of the pressure-volume relationship measured during afterload stress and left ventricular ejection fraction response to exercise intervention more reliably reflect the degree of left ventricular dysfunction.

Adult↗
PubMed1985

Influence of coronary collateral blood flow on the development of exertional ischemia and Q wave infarction in patients with severe single-vessel disease.

The functional significance of coronary collateral flow from a nonobstructed supply artery was studied in 121 patients with severe (greater than or equal to 80%) single-vessel disease, 64 with and 57 without Q wave infarction. All patients underwent exercise thallium imaging and coronary angiography. On angiography, collateral flow was present in 85% of 74 occluded arteries compared with only 17% of 47 arteries with subtotal obstruction (p less than .001). Collateral flow was not seen in arteries with lesions of less than 90% obstruction. Collateral flow was present in 100% of 29 occluded arteries in patients without Q wave infarction compared with only 76% of 45 occluded arteries with Q wave infarction (p less than .005). Clinical variables did not correlate with collateral flow. Collateral flow did not prevent ischemia on exercise thallium imaging in patients without Q wave infarction: 30 of 33 (91%) with collateral flow had reversible thallium defects compared with 24 of 24 (100%) without collateral flow (p = NS). In patients with Q wave infarction, partially reversible exercise thallium defects (peri-infarctional ischemia) were more common with flow to the area from either subtotal obstruction (73%) or collateral flow (45%) than with no flow from total occlusion (27%; p = .05). In patients with severe single-vessel disease the presence of collateral flow is principally determined by coronary occlusion. Collateral flow may protect from Q wave infarction but does not prevent exercise ischemia on thallium imaging.

Adult↗
PubMed1985

Effects of nifedipine on systemic and regional oxygen transport and metabolism at rest and during exercise.

In a placebo-controlled, randomized, cross-over, double-blind study of 12 patients with stable exertional angina, we measured at rest and during bicycle exercise the effects of 20 mg of nifedipine administered sublingually on hemodynamics and systemic and regional oxygen extraction and metabolism. Nifedipine decreased systemic vascular resistance by 38% at rest (p less than .001) and by 28% during exercise (p less than .001). Cardiac output increased from 4.6 +/- 0.6 to 6.0 +/- 0.9 liters/min (p less than .001) at rest after nifedipine and from 10.6 +/- 3.7 to 11.8 +/- 3.4 liters/min (p less than .005) during exercise. After nifedipine, the arterial-mixed venous O2 content difference decreased from 4.7 +/- 0.6 to 3.5 +/- 0.5 ml/100 ml (p less than .001) at rest and from 10.5 +/- 1.7 to 8.8 +/- 1.6 ml/100 ml (p less than .001) during exercise. After nifedipine the arterial-iliac venous O2 content difference also decreased at rest, from 5.9 +/- 1.5 to 4.8 +/- 1.7 ml/100 ml (p = .06) but increased during exercise from 13.1 +/- 1.5 to 14.0 +/- 1.8 ml/100 ml (p less than .05). Oxygen consumption was not significantly altered at rest or during exercise. Nifedipine decreased mixed venous carbon dioxide tension (PCO2) during exercise from 53 +/- 3.5 to 50 +/- 4.0 mm Hg (p less than .05) but increased iliac venous PCO2 slightly from 61 +/- 4.6 to 63 +/- 5.2 mm Hg (p less than .01). Exercise pH was not significantly altered, but arterial lactate increased more after nifedipine (2.65 +/- 1.95 mmol/liter placebo, 3.54 +/- 2.74 mmol/liter nifedipine; p less than .05). Thus nifedipine produces similar changes in O2 extraction in mixed venous and iliac venous blood at rest but directionally opposite changes during exercise. The data support the hypothesis that nifedipine does not alter the distribution of cardiac output to the legs at rest, but during dynamic leg exercise reduces the redistribution of cardiac output to the legs. This probably results from the shunting of blood flow away from exercising muscles by the generalized vasodilatation of nifedipine.

Angina Pectoris↗
PubMed1984

Abnormal left ventricular response to isometric exercise in pure, isolated aortic regurgitation: beneficial effects of nifedipine.

To examine the effects of nifedipine on the left ventricular (LV) functional response to isometric exercise in patients with aortic regurgitation (AR), 20 patients with isolated, moderate to severe AR performed 3 minutes of handgrip exercise at 33% of their maximal voluntary contraction, before and after administration of 20 mg of sublingual nifedipine. Although handgrip exercise produced similar increases in heart rate and systolic blood pressure before and after nifedipine treatment, heart rate was higher and systolic blood pressure lower with handgrip exercise during nifedipine treatment. LV end-diastolic volume index was not different during the control period and nifedipine handgrip exercise, but the increase in end-systolic volume index was smaller and the ejection fraction was higher during nifedipine handgrip exercise. Nifedipine reduces afterload and ameliorates handgrip exercise-induced LV dysfunction in patients with AR.

Adult↗
PubMed1984

Anterolateral ST segment depression in acute inferior myocardial infarction: angiographic and clinical implications.

We examined the relationship between coronary anatomy and anterolateral ST segment depression during inferior acute myocardial infarction (AMI) in 84 consecutive survivors of inferior AMI, who underwent prospective coronary angiography a median time of 2 weeks after AMI. Multivessel disease was defined as two or more significantly (greater than 70%) stenosed vessels. A QRS scoring system was used to estimate myocardial infarct size. Patients with ST depression had more multivessel disease compared to patients with no ST depression (53% vs 6%, p less than 0.01), more left anterior descending stenoses (36% vs 10% p less than 0.05), and higher QRS scores (5.8 +/- 3.2 vs 2.6 +/- 1.8, p less than 0.01) indicating larger infarcts. Patients with ST depression and one-vessel disease (47%) still had higher QRS scores compared to patients with no ST depression (4.8 +/- 2.9 vs 2.6 +/- 1.8, p less than 0.001) and had an increased prevalence of infarct-related vessels with a terminal branch supplying the left ventricular lateral wall or apex. We conclude that anterolateral ST depression during inferior AMI may indicate the presence of additionally stenosed vessels or that the infarct-related vessel has a large vascular territory. The absence of ST depression virtually precludes multivessel disease.

Adult↗
PubMed1984

Noninvasive assessment of acute effects of nifedipine on rest and exercise hemodynamics and cardiac function in patients with aortic regurgitation.

The acute effects of nifedipine (20 mg sublingually) on hemodynamics and cardiac function were studied at rest and during supine bicycle exercise in 20 patients with aortic regurgitation. At rest, heart rate increased by 13%, systemic vascular resistance decreased by 34% and regurgitant index decreased by 17%. The change in systemic vascular resistance was related to its initial rest level (r = 0.82, p less than 0.001) and to the changes in forward cardiac output (r = 0.58, p less than 0.01) and regurgitant index (r = 0.60, p less than 0.01). Left ventricular end-diastolic and end-systolic volumes, stroke volume and ejection fraction were unchanged, whereas right ventricular ejection fraction increased. During exercise, nifedipine administration further increased heart rate by 8% and decreased systemic vascular resistance by 19%. Both forward stroke volume and forward cardiac output increased, but total left ventricular stroke volume was unchanged, resulting in a significant decrease in regurgitant index. Although left ventricular end-diastolic volume was slightly decreased, end-systolic volume did not increase; thus, ejection fraction was higher than that during control exercise (p less than 0.01). Right ventricular ejection fraction increased further. In aortic regurgitation, the acute administration of nifedipine improved cardiac performance and reduced regurgitation at rest and during exercise as a result of afterload reduction and increased heart rate. Whether these beneficial effects will occur during long-term therapy requires further investigation.

Adult↗
PubMed1984

Effects of intravenous verapamil on the haemodynamic response to exercise in patients with angina pectoris.

The effects of intravenous Verapamil (V) on exercise haemodynamics and ventricular function were compared in 13 patients with stable effort angina. Intravascular pressures, thermodilution cardiac output and radionuclide ejection fraction were measured simultaneously at rest and during exercise. At rest Verapamil produced systemic vasodilation. During exercise at identical workloads compared to control, Verapamil increased cardiac index (CI) and decreased AVO2 difference. Pulmonary artery wedge pressure was lower. Ejection fraction was higher (control-55 +/- 11% vs V-64 +/- 11%) as the disproportionate increase in end systolic volume relative to the end diastolic volume was prevented. Verapamil is effective in exercise induced angina and alters haemodynamics primarily through its vasodilating properties associated with an increased CI.

Adult↗
PubMed1984

The clinical features of isolated left circumflex coronary artery disease.

The clinical characteristics of 84 patients with isolated circumflex disease (greater than or equal to 70% luminal stenosis) were reviewed. A total of 66 patients had angina pectoris (mean duration 17.3 months), and 60 had suffered a myocardial infarction. Risk factors averaged 2.2 per patient. In the 84 patients there were 103 discrete circumflex stenoses; 51 stenoses were central (proximal circumflex, obtuse marginal, and intermediate branches), and 52 were peripheral (distal circumflex, posterolateral, and posterior descending branches); 48 were total and 55 were subtotal. Left ventricular function was normal in 21 patients and abnormal in 63 patients, but the mean left ventricular ejection fraction of the group was normal (59 +/- 12%). Eighty-two patients had abnormal electrocardiograms: there were Q waves in 25, RV pattern in 43, ST-T wave abnormalities in 19, left bundle branch block in two, and pacemaker rhythm in one. Inferior abnormalities on the electrocardiogram correlated with peripheral stenoses (p less than .02), and lateral abnormalities on the electrocardiogram correlated with central stenoses (p less than .01). The RV pattern of true posterior infarction was seen in both central and peripheral stenoses. In the 32 patients who underwent thallium scanning, lateral defects were more common with central stenoses, but posterolateral defects occurred similarly in central and peripheral stenoses. Prognosis was good. There were two deaths during the mean follow-up time of 17 months (range 1 to 49). The cumulative survival rate was 100% at 12 months, 97.5 +/- 2.9% at 24 months, and 97.5 +/- 3.6% at 30 months.

Adult↗
PubMed1984

Beta-adrenergic stimulation of the failing ventricle: a double-blind, randomized trial of sustained oral therapy with prenalterol.

Eleven patients with severe left ventricular impairment (mean ejection fraction 24%) and moderate impairment of exercise tolerance underwent a double-blind, placebo-controlled, cross-over trial of the orally administered beta-agonist prenalterol. Exercise hemodynamics and tolerance were measured during bicycle and treadmill exercise after 2 weeks of therapy with placebo or prenalterol. Cardiac index, ejection fraction, and stroke work index were not improved and exercise duration and peak oxygen consumption were not significantly different during the two treatments. During prenalterol treatment heart rate during exercise was consistently reduced. These results show that prolonged therapy with prenalterol does not improve hemodynamics or exercise tolerance and is associated with a diminished heart rate response to exercise.

Administration, Oral↗
PubMed1983

Prognosis after an initial non-Q-wave myocardial infarction related to coronary arterial anatomy.

Eighty-six consecutive hospital survivors (aged less than or equal to 60 years) of a first non-Q-wave acute myocardial infarction (MI) were followed up prospectively. Coronary arteriography was performed a median of 2 weeks after MI. The size of the MI was small (as judged by a mean peak creatine kinase level of 906 IU/liter); 90% were in Killip class I, and the mean left ventricular ejection fraction was 60 +/- 11% (+/- standard deviation). Forty-nine patients had 1 vessel significantly narrowed by disease (greater than or equal to 70% luminal diameter reduction), 19 had 2-vessel, 2 had 3-vessel, 3 had left main (greater than or equal to 50% luminal diameter reduction), and 13 minimal or no coronary artery disease (CAD). Complete occlusion of the MI-related vessel was present in 33 patients. All 33 and an additional 5 patients had collateral vessels to the MI area. During a mean follow-up of 25 months, 1 cardiac death and 4 recurrent infarcts (3 with non-Q-wave MI) occurred. Angina occurred in 53 patients (62%) and responded medically in all but 7 who underwent coronary artery surgery. Angina after MI occurred frequently in patients with severe proximal left anterior descending CAD (greater than or equal to 90%), and in those with CAD (greater than or equal to 50%) in a vessel supplying collaterals to the infarct area. Because angina can be managed medically in most patients and the outcome is good, routine coronary angiography is not indicated in asymptomatic survivors less than or equal to 60 years of a first non-Q-wave MI.

Angina Pectoris↗
PubMed1983

Clinical studies of patients with coronary spasm.

Coronary artery spasm may cause myocardial ischemia in patients without severe coronary atherosclerotic obstruction. Spontaneous rest angina, particularly at night, is the predominant symptom; most patients are smokers. Ergonovine tests have high sensitivity and specificity for the diagnosis of coronary spasm, but should be used when vasospasm is suspected but no electrocardiogram was recorded during spontaneous angina. Arterial constriction measured during ergonovine testing suggests that the arterial hypersensitivity to vasoconstrictors at sites of atherosclerotic lesions is independent of the severity of the lesion. Coronary vasospasm may also be provoked by exercise, possibly through an alpha-adrenergic mechanism. Both spontaneous and exercise-induced attacks of vasospasm are prevented by calcium-antagonist drugs that remain effective during longer-term treatment. The cyclic nature of the condition is demonstrated when successful therapy is discontinued without recurrence of symptoms and may be due to alteration of arterial hypersensitivity.

Angina Pectoris↗
PubMed1983

Coronary and left ventricular angiographic anatomy and prognosis of survivors of first acute myocardial infarction.

To relate coronary anatomy and left ventricular function to prognosis, 197 of 269 consecutive survivors of a first myocardial infarction (MI) less than or equal to 60 years old underwent prospective cardiac catheterization a median of 2 weeks after admission and were followed up for a median of 24 months (range 12 to 61). Seventy-two patients were excluded from angiography because of early death (9), severe noncoronary disease (44), MI complications (6), or patient refusal (13). The prevalence of multivessel disease was low (30%) and unrelated to the site of MI or presence of Q waves but was increased in patients with previous angina pectoris (p = 0.05) or those in Killip class II or III (p = 0.02). There were only 8 deaths from heart disease. The survival rate at 12 months was 97 +/- 1% and at 24 and 36 months, 95 +/- 2%. Nineteen patients underwent coronary revascularization surgery. As the number of deaths was small, the differences in survival between patients with single or multivessel disease and normal or depressed ejection fractions failed to reach significance. Survivors of a first MI less than or equal to 60 years old have a low prevalence of multivessel disease and a good prognosis.

Adult↗