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Biomedical subjects

M W Cleman

Publications and source records attributed to M W Cleman.

28 records · Page 2Linked to original sources
PubMed1989

Predictors of success in percutaneous transluminal coronary angioplasty of chronic total occlusions.

Earlier studies have indicated that percutaneous transluminal coronary angioplasty (PTCA) of chronic total occlusions has a low success rate. To determine success rate and assess clinical and angiographic variables associated with success and complications, 57 total occlusions in 56 patients undergoing PTCA were analyzed. The clinical duration of occlusion was 51 +/- 86 days. Success (less than 50% residual stenosis) was achieved at 40 of 57 (70%) dilatation sites. Of these 57 total occlusions, 5 were attempted within 24 hours of acute myocardial infarction, 35 between 1 day and 8 weeks of clinical occlusion, 13 greater than 8 weeks and 4 were of unknown duration. Success rates were 4 of 5, 25 of 35, 9 of 13 and 2 of 4, respectively, in each group (difference not significant, comparison of all time groups). Of the 9 narrowings with a successful PTCA for an occlusion greater than 8 weeks, the mean duration of occlusion was 93 +/- 41 days (range 60 to 180). None of the attempted dilatations of occlusions with a clinical duration of greater than 180 days (n = 3) was successful. None of the clinical or angiographic variables (including tortuosity, length of occlusion gap, distance of the occlusion from the vessel origin, thrombus, lesion calcium, collaterals, prior myocardial infarction, vessel dilated or diffuse disease) impacted on success rate (difference not significant for all). No patient died, had a Q-wave infarction, required emergency coronary artery bypass grafting or underwent repeat PTCA within 7 days of the procedure. Non-Q-wave infarction occurred in 2 of 56 patients (4%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Pulmonary and pleural complications of cardiac disease.

Disorders of the heart frequently cause pulmonary dysfunction because of the close structural and functional association of the heart and lungs. The pulmonary vasculature is very commonly affected by cardiac pathology. The pulmonary vasculature is normally a low-pressure, low-resistance circuit with high compliance and tremendous vascular reserve. Although resting vascular tone is low, there are many identified mediators of pulmonary arterial tone that may help mediate pulmonary blood flow. Alveolar hypoxia is clearly a stimulus for increasing pulmonary vascular resistance although factors that mediate the response to hypoxia are not fully understood. Patients with left-to-right shunting due to congenital heart disease because of elevations in pulmonary artery flow and pressure tend to develop progressive anatomic changes in the pulmonary vasculature. This leads to an increase in pulmonary vascular resistance, irreversible pulmonary hypertension, right heart failure, reversal of shunt flow, and Eisenmenger's syndrome. The degree of anatomic vascular damage due to left-to-right shunting can be graded histologically. Lesser grades of damage are reversible with corrective surgery, whereas more severe grades show no improvement or progression with operation. Chronic left-sided congestive heart failure seen in rheumatic mitral stenosis can cause secondary changes in the pulmonary vasculature. Pulmonary hypertension and increased pulmonary vascular resistance can increase reflexly and form a "second stenosis" that further limits cardiac output. Unlike congenital heart disease, severe grades of pulmonary arterial damage are not seen in left heart failure from mitral stenosis or other causes, and consequently with surgical correction pulmonary hypertension reverses. Pulmonary function testing is adversely affected by congestive heart failure. Both restrictive (stiff lungs) and obstructive (cardiac asthma) defects are observed in congestive heart failure. DLCO is abnormally decreased. With treatment of heart failure these defects reverse. Both elevated systemic and pulmonary venous pressures affect fluid filtration in the pleural space and cause pleural fluid accumulation. The fluid is transudative with low protein, low lactate dehydrogenase, and low cell counts. Transudative effusions from heart failure resolve with treatment. With large effusions and cardiomegaly, pulmonary dysfunction results because of atelectasis from compression and space-occupying effects of the heart and pleural fluid. Following myocardial infarction, cardiac surgery, or other cardiac trauma, the postcardiac injury syndrome can result. The syndrome is characterized by exudative pleural and pericardial effusions along with pulmonary infiltrates, fever, chest pain, leukocytosis, and an elevated ESR. The syndrome must be diagnosed by exclusion of bacterial pneumonia, pulmonary emboli, and congestive heart failure. Treatment is with nonsteroidal anti-inflammatory agents or systemic co

Cardiovascular Agents↗
PubMed1988

Dynamics of early and late left ventricular filling determined by Doppler two-dimensional echocardiography during percutaneous transluminal coronary angioplasty.

To study the influence of ischemia on both early and late left ventricular filling, Doppler 2-dimensional echocardiography was used to measure filling parameters during percutaneous transluminal coronary angioplasty (PTCA) in 26 patients. Doppler recordings were taken immediately before balloon inflation and continuously during balloon inflation and deflation until 60 seconds into the recovery period. During PTCA of the left anterior descending artery (16 patients) there was a 35% decrease in early peak filling rate from 269 +/- 88 to 169 +/- 55 ml/s (p less than 0.0005) by 60 seconds of balloon inflation. In patients undergoing PTCA of the left circumflex (4 patients) or dominant right coronary artery (6 patients), the early peak filling rate decreased 15% from 325 +/- 126 to 284 +/- 137 ml/s (p less than 0.005). The decrease in early peak filling rate became evident at approximately 15 seconds after balloon inflation and fully recovered 20 seconds after balloon deflation. Rather than an expected increase in atrial stroke volume and a decrease in early to late filling ratio during coronary occlusion, there was a 28% decrease in atrial stroke volume during left anterior descending coronary artery PTCA and a 6% decrease during right coronary and circumflex PTCA. Because of the simultaneous decrease in both early and late ventricular filling, peak early to late filling ratio was only slightly altered during PTCA. There was an 83% increase in mean pulmonary artery wedge pressure during balloon inflation from 12 +/- 5 to 20 +/- 4 mm Hg. In 11 of these patients global systolic function was measured on subsequent inflations during PTCA using 2-dimensional echocardiography.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Percutaneous transluminal coronary angioplasty during acute myocardial infarction.

Intravenous thrombolytic therapy with streptokinase in the setting of acute MI has been shown to be effective in improving left ventricular function, limiting infarct size, and improving early mortality. The benefit of this therapy is greatest when administered within 3 hours and is of minimal benefit when given more than 6 hours from symptom onset. Newer second generation thrombolytic agents such as intravenous r-TPA have been shown to be more effective at establishing patency of acutely thrombosed coronary arteries. TPA treatment produces patency rates similar to those observed with intracoronary administration of streptokinase (65 to 75 per cent). This agent will probably become standard therapy for patients with acute MI. Unfortunately, there are significant problems with systemic thrombolytic therapy. The potential for bleeding complications contraindicates the use of this therapy in patients with recent cerebrovascular events, recent surgery, or other possible bleeding problems. Acute angioplasty of the infarct-related artery has been shown to be effective in restoring blood flow in 85 per cent of patients with acute MI. Preliminary studies have suggested that this therapy, when administered within 4 hours from symptom onset, improves global and regional left ventricular function to a greater degree than intracoronary streptokinase. Patients receiving acute PTCA as a primary reperfusion modality have a lower incidence of post-infarction angina and provokable ischemia by exercise testing. If facilities and skilled personnel are available to perform PTCA within 4 hours from symptom onset, this therapy remains an alternative revascularization modality in patients with acute infarction and contraindications to systemic thrombolytic therapy. However, the benefit of PTCA with regard to reduction in mortality when used in this manner is unproven. PTCA can also be used as an adjunctive therapy administered at some time following systemic thrombolytic therapy. Performing PTCA acutely offers the potential to restore blood flow in 90 per cent of the patients that initially fail thrombolytic therapy. However, despite the use of PTCA in this subgroup, benefits with regard to improved ventricular function and decreased mortality have yet to be conclusively demonstrated. Performing acute PTCA following systemic thrombolytic therapy also incurs a high incidence of bleeding complications. If initial thrombolytic therapy reestablishes vessel patency, similar improvements in ventricular function can be expected even if PTCA is deferred until clinically indicated by evidence of recurrent ischemia.(ABSTRACT TRUNCATED AT 400 WORDS)

Angioplasty, Balloon↗
PubMed1988

Update on percutaneous transluminal coronary angioplasty.

Percutaneous transluminal coronary angioplasty was first performed in a human coronary artery in 1977. In this article, we review the possible mechanisms of angioplasty, current indications for angioplasty, and complications of angioplasty including acute closure and restenosis.

Angioplasty, Balloon↗
PubMed1981

Insulin degradation in serum of a patient with apparent insulin resistance.

A case is presented of a thin diabetic male who was resistant to large doses of sc and im insulin but responded to small dose of insulin given iv. His serum contained an enzyme that degraded [125I]insulin in vitro. We postulate that his apparent insulin resistance was due to inactivation of insulin at the injection site. We propose that the sera of patients with insulin resistance be tested for [125I]insulin-degrading activity as a possible means of identifying patients with this syndrome.

Adult↗