PTCA in elderly patients: hospital events.

BACKGROUND: Medical treatment of the elderly is changing to include the aggressive management of coronary artery disease with percutaneous transluminal coronary angioplasty. OBJECTIVE: The purpose of this study was to review major hospital events of patients aged 70 years or more, who underwent a first percutaneous transluminal coronary angioplasty. METHODS: A retrospective medical record review was done of 246 consecutive patients of 70 years or more, from January 1985 to December 1988, at a tertiary care community hospital. Adverse events and the factors that influenced outcome were identified. RESULTS: Of 246 patients (age range, 70-85 years, mean = 73.6), 19 died, 4 had a cerebral vascular accident, 11 had a transfusion and 11 underwent coronary artery bypass grafting. Sixteen patients had acute vessel closure and 8 died. Twenty-five patients had one event and 21 patients had more than one. DISCUSSION: The event rate after percutaneous transluminal coronary angioplasty in the elderly is high. CONCLUSIONS: Knowledge of the factors that influence adverse events (diagnostic category, success of procedure, degree of coronary artery disease and age) will assist the critical care team to plan and implement appropriate care.

Effect of intracoronary nifedipine on coronary bloodflow and myocardial metabolism during pacing-induced ischemia.

The effects of intracoronary nifedipine on coronary bloodflow, its regional distribution, myocardial oxygen consumption and lactate metabolism during pacing-induced angina were evaluated in 15 subjects. These responses were directly compared to 10 subjects who received an alcohol-based control solvent. Myocardial bloodflow was measured by thermodilution, with changes in regional coronary flow assessed using a dual radiolabelled (technetium-99m and indium-111) intracoronary microsphere technique and single photon emission tomography. Neither intracoronary nifedipine (100 micrograms) or the control solvent produced changes in systemic arterial pressure (nifedipine -2 mmHg and control +2 mmHg, both not significant). Intracoronary nifedipine markedly increased left ventricular end diastolic pressure (pre-nifedipine 13.0 mmHg versus post nifedipine 20.1, P less than 0.05), while increasing total coronary sinus bloodflow (pre-nifedipine 134 mL/min versus post nifedipine 189, P less than 0.05): Regional coronary bloodflow increased in all myocardial segments, regardless of the severity of coronary stenosis (64 to 132% baseline, all P less than 0.05). In addition, intracoronary nifedipine increased myocardial oxygen consumption (pre-nifedipine 12.3 mL/min versus post nifedipine 15.7, P less than 0.05), with a trend towards improved lactate extraction (pre-nifedipine 0.24 mg/mL versus post nifedipine 0.12, not significant). Although decreased ventricular afterload (left ventricular systolic wall stress) may contribute to nifedipine's antianginal properties, a primary increase in regional coronary bloodflow also appears to be an important factor in the alleviation of myocardial ischemia.

Validation of left ventricular function parameters acquired with the non-imaging nuclear probe: comparison with tantalum marker cine-fluoroscopy.

We evaluated the accuracy of the non-imaging nuclear probe for measuring various parameters of left ventricular function by comparing these with simultaneous measurements acquired via tantalum marker cine-fluoroscopy. Eight patients with surgically implanted mid-myocardial tantalum markers were studied during cardiac catheterization. High temporal resolution tantalum marker-derived volume/time curves were generated and calibrated to absolute endocardial volumes by comparison with contrast left ventricular angiography. Left ventricular function parameters were acquired at baseline and during atrial pacing, nitroprusside infusion and volume loading. Simultaneous measurements obtained with the nuclear probe and via tantalum marker cine-fluoroscopy were compared. The following correlation coefficients were obtained: ejection fraction, r = 0.49, P less than 0.001; peak ejection rate, r = 0.41, P less than 0.01; mean ejection rate, r = 0.62, P less than 0.001; time to peak ejection, r = 0.73, P less than 0.001; peak filling rate, r = 0.73, P less than 0.001; time to peak filling, r = 0.58, P less than 0.001. Relative changes in end-diastolic volume were accurately tracked by the nuclear probe in six of seven patients (r values 0.77-0.93). These results suggest that measurements of certain left ventricular volume parameters with the nuclear probe may not accurately reflect true volume changes as measured by tantalum marker cine-fluoroscopy. Although, the probe may be useful in tracking relative changes in end-diastolic volume, we would advise caution in using this instrument for studies requiring accurate measurements of ejection and filling parameters.

Abnormal thallium kinetics in postoperative coarctation of the aorta: evidence for diffuse hypertension-induced vascular pathology.

After operative correction of congenital coarctation of the aorta, patients continue to have excess cardiovascular mortality, including manifestations of ischemic heart disease. Previous morphologic studies support the concept of direct hypertensive vascular injury in these patients. To determine whether abnormalities of myocardial perfusion were present in an asymptomatic group of patients with coarctation repair, 18 men and 9 women with a mean age of 26 years (range 19 to 41) were studied between 2 and 25 years after operative correction. Stress electrocardiography and quantitative thallium imaging by a circumferential profile technique were used. These patients were compared with a normal group, statistically defined as having a less than 1% prevalence of significant obstructive coronary artery disease. The postoperative coarctation group demonstrated a reduction in global thallium redistribution in each view analyzed. As compared with findings in the control subjects, thallium washout in the anterior view (41.9 versus 48.6%, p = 0.02) and left anterior oblique projection (40.5 versus 48.2%, p = 0.007) was significantly diminished. Although the postoperative coarctation group had a lower thallium redistribution rate in the lateral view (41.4 versus 46.3%, p = 0.09) this difference did not reach statistical significance because of the intrinsic variability of this projection. Plots of the median percent thallium washout revealed independence from circumferential profile angle, indicating global abnormalities in perfusion. No correlation between clinical variables and thallium kinetics could be established, suggesting marked individual variability in the development of this vascular lesion. The observation of abnormal thallium kinetics in patients with coarctation repair may have consequences for long-term follow-up and therapy.

Clinically unrecognized ventricular dysfunction in young diabetic patients.

Left ventricular function at rest and during supine bicycle exercise was assessed by gated radionuclide angiography in 20 diabetic patients and 18 normal control subjects without clinical evidence of heart disease. The diabetic patients were aged 21 to 44 years and all except one used insulin. No subject developed chest pain or electrocardiographic changes during exercise. Both groups had a similar rest and exercise heart rate and blood pressure, and both achieved similar work loads. The control group had an ejection fraction at rest of 65.4 +/- 6.2% (mean +/- SD) and only 1 of 18 showed a decrease with exercise; peak exercise ejection fraction averaged 77.1 +/- 7.8%. The diabetic group had a mean ejection fraction at rest of 63.7 +/- 6.5%, similar to that of the control group, but 7 of 20 showed a decrease during exercise; the exercise ejection fraction averaged 67.7 +/- 9.7%, significantly lower than that of the control group (p less than 0.01). The diabetic patients varied widely in ejection fraction response to exercise, ranging from an increase of 25% to a decrease of 21%. This response did not correlate with age, sex, duration of diabetes, smoking, retinopathy, exercise heart rate, blood pressure or rate-pressure product, work load attained or ejection fraction at rest. These data suggest that approximately one-third of patients with diabetes have subclinical left ventricular dysfunction without correlation to risk factors for atherosclerosis or other diabetic complications. Whether this is due to unrecognized coronary artery disease or primary myocardial disease remains unknown.

Role of autoregulation in spatial and temporal perfusion heterogeneity of canine myocardium.

Spatial heterogeneity, the region-to-region variation in flow at an instant, and temporal heterogeneity, the time variation of flow in a small region of myocardium, were investigated with radioactive labeled microspheres in 111 regions of left ventricular myocardium. The error of the method was measured by simultaneously injecting four differently labeled microspheres (15 +/- 5 (SD) micron). The coefficient of variation (CV) was 6.5 +/- 1.0%. Spatial variation with autoregulation intact was 21.7 +/- 1.4% (CV); with autoregulation abolished and low perfusion pressure, it was 34.3 +/- 3.7%; and with normal perfusion pressure, 30.8 +/- 6.4% (differences not significantly). This degree of variation was similar in the entire left ventricle and its layers. Forces which tended to cause vessel closure (low perfusion pressure, ventricular systolic pressure, and ventricular diastolic pressure) tended to increase CV. Temporal heterogeneity as measured by 20-s intervals between microsphere injections was 11.1 +/- 1.0% (CV) with autoregulation, 9.8 +/- 1.3% (P less than 0.05) with autoregulation abolished, and 8.4 +/- 0.8% (P less than 0.05) when perfusion pressure was restored. A periodicity of flow cycles of 30-90 s was suggested by the data. These results suggest that spatial heterogeneity is less influenced by autoregulation than by hydraulic considerations, whereas temporal heterogeneity is a component of autoregulation.

Redistribution in left ventricular regional flow following acute right ventricular pressure overload.

The left ventricular dysfunction following acute pulmowary hypertension remains unexplained. We wondered if acute pulmonary hypertension could alter the transmural flow distribution within the left ventricular myocardium, independent of coronary flow and perfusion pressure. We used a canine preparation in which the left coronary system was perfused at constant flow and induced a two- to three-fold increase in pulmonary artery pressure by banding the pulmonary artery. Regional myocardial blood flow of the left coronary system was measured using radioactive microspheres, injected into the left coronary system before and after 10-30 min of banding of the pulmonary artery. The left ventricular subendocardial:epicardial ratio fell by 12 and 31% (p less than 0.05) of control value, 10 and 30 min, respectively, after banding of the pulmonary artery, the total flow to the left coronary system being kept constant. Left atrial mean pressure increased from 2.9 +/- 2.4 to 3.6 +/- 1.9 and 6.0 +/- 2.1 (p less than 0.05) following banding. The mechanism of the redistribution of coronary flow may relate to inappropriate vasodilation of the right septal myocardium with consequent relative left ventricular subendocardial hypoperfusion which might aggravate left ventricular ischemia in the presence of hypotension and hypoxia.

The role of coronary flow and pressure as determinants of myocardial oxygen consumption in the presence or absence of vasomotor tone.

When coronary flow was kept constant and coronary pressure increased by angiotensin or decreased by dipyridamole, myocardial oxygen consumption (MVO2) remained unchanged. When vasomotor tone was abolished by dipyridamole or was intact, changing coronary flow resulted in a change in MVO2 in the same direction as flow; this change in MVO2 was in part the result of a significant alteration in coronary oxygen extraction. These results suggest that coronary flow, but not coronary pressure is an important determinant of MVO2 both in the presence or absence of vasomotor tone.

The relationship between oxygen extraction and extravascular mean transit time in the canine heart.

A significant relationship was observed between myocardial oxygen extraction and the extravascular mean time transit time. This relationship implies that oxygen extraction by the myocardium is a time-dependent process, and emphasizes the critical link between blood flow and myocardial oxygen consumption.

Myocardial tissue recruitment in the dog as determined by double tracer dilution method.

The amount of tissue perfused, as determined from the difference in volume of distribution between a diffusible indicator (125I-antipyrine) and an intravascular indicator (131 I-albumin) was measured at different values of coronary flow, perfusion pressure, and vasomotor tone in the working left ventricle of an open-chest dog. Coronary pressure and flow were regulated independently from the systemic circulation and coronary vasomotor tone was reduced by dipyridamole. At each flow vasomotor tone was assessed by using as a reference the maximal vasodilation induced by arrest of flow. Measured tissue space was considered to be related to the capillary surface area available for tracer diffusion and therefore to the number of perfused capillaries per volume of muscle. A relationship between coronary blood flow and tissue volume was observed. It was found to be independent of vasomotor tone. Vasodilation was found to increase available exchanging capillary surface at a constant perfusion pressure.

Effects of perhexiline maleate on coronary flow distribution in the ischemic canine myocardium.

Intravenous perhexiline maleate in a canine preparation with fixed coronary flow increases coronary diastolic pressure. It also redistributes coronary flow so as to preserve endocardial flow. Myocardial oxygen consumption was reduced and lactate uptake enhanced by the drug. It had no effect upon the threshold for ischemic-induced left ventricular failure.

The effect of acetazolamide on myocardial carbon dioxide space.

Carbon dioxide, water and vascular space were measured in the heart muscle of the dog before and after the administration of acetazolamide. In contrast to the skeletal muscle whose CO2 space was markedly reduced by acetazolamide, cardiac muscle CO2 space was only minimally reduced. This suggests that cardiac muscle does not have extravascular carbonic anhydrase. Its presence in skeletal muscle and absence in cardiac muscle probably relates to the differences in cell size between the two types of muscle and their differing degree of vascularity.