Percutaneous revascularization for unstable angina in the elderly.
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Biomedical subjects
Publications and source records attributed to K P Marzo.
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Bacteremia after diagnostic cardiac catheterization is uncommon, but bacteremia after percutaneous transluminal coronary angioplasty (PTCA) has not been studied prospectively. Unlike diagnostic cardiac catheterization, PTCA involves the use of an indwelling arterial sheath after completion of the procedure, which is connected to a pressurized heparin solution, both of which increase the risk of local infection and/or bacteremia. During a 16-week period, we prospectively evaluated patients undergoing 164 PTCA procedures in order to determine the frequency of bacteremia and the significance of fever in this patient population. Blood cultures were obtained from the femoral catheter at the conclusion of the procedure and again 30 min later from the indwelling arterial sheath. Temperature was recorded every 30 min for 2 h following PTCA, then every 4 h over the subsequent 36-hr period. Bacterial isolates were recovered from 23/286 blood cultures (8.0%), with Staphylococcus epidermidis the most common organism present (74%). Only one isolate of Staphylococcus aureus was considered to represent true bacteremia and corresponded with the only documented infectious complication. Fever, defined as > or = 101 degrees F developed in four (2.4%) patients but was procedure related in only one case. The use of the ipsilateral femoral artery for repeat procedures was not associated with either positive blood cultures or difference in maximum temperature elevation. We conclude the overall risk of bacteremia after PTCA is low; therefore, antimicrobial prophylaxis is not warranted.
Superior vena caval syndrome (SVC) following transvenous pacemaker insertion is an uncommon complication that has been treated with percutaneous transluminal balloon angioplasty. We report a case of SVC syndrome following pacemaker implantation that was treated with angioplasty. Several days after the initial balloon dilation, the patient had recurrent symptoms and evidence of restenosis on catheterization. Following repeat balloon dilation of this restenotic lesion, the patient had a favorable clinical response evidenced on hemodynamic and angiographic follow-up at 6 months.
OBJECTIVES: The short- and long-term effects of valvuloplasty on exercise capacity, ventilation and skeletal muscle oxygenation were investigated to determine whether a dissociation between hemodynamic improvement and exercise capacity occurs in patients with mitral stenosis. BACKGROUND: Percutaneous balloon mitral valvuloplasty in patients with mitral stenosis results in immediate hemodynamic improvement at rest and with exercise. Improved exercise capacity has been described at 3 months after valvuloplasty. In patients with left ventricular dysfunction, acute therapeutic interventions that produce hemodynamic benefit do not immediately improve exercise capacity. METHODS: Maximal bicycle exercise with measurement of respiratory gases was performed in 11 patients with mitral stenosis before and at 48 h and 3 months after successful percutaneous balloon mitral valvuloplasty. Respiratory and leg skeletal muscle oxygenation were assessed by monitoring changes in light absorption of the serratus anterior and vastus lateralis muscles using near-infrared spectroscopy and were expressed as percent deoxygenation. RESULTS: Mitral valvuloplasty significantly increased mean mitral valve area from 1.0 +/- 0.2 to 1.7 +/- 0.3 cm2 (p < 0.05). Immediately after valvuloplasty, peak exercise oxygen consumption (VO2), VO2 at the anaerobic threshold, ventilation, peak respiratory and leg muscle deoxygenation all remained unchanged. At submaximal work loads, respiratory muscle deoxygenation was attenuated (25 W: before 12 +/- 4%; 48 h 4 +/- 3%; 50 W: before 10 +/- 5%; 48 h 5 +/- 4%; both p < 0.05). At 3 months, significant improvement in peak VO2 (before 10.9 +/- 5%; 3 months 14.6 +/- 6.2 ml/kg per min; p < 0.05) and VO2 at the anaerobic threshold (before 7.1 +/- 2.4; 3 months 8.4 +/- 2.3; p < 0.05) were observed, whereas ventilation remained unchanged. No further improvement was seen in respiratory muscle deoxygenation. Vastus lateralis deoxygenation at submaximal work loads tended to be decreased. CONCLUSIONS: Long-term changes in skeletal muscle and the lungs preclude immediate enhancement of exercise performance after balloon mitral valvuloplasty. Immediate symptomatic improvement probably results from an immediate decrease in the work of breathing. Long-term symptomatic improvement results from changes that occur in the peripheral skeletal musculature as well as from the reduced work of breathing.
As patients survive to advanced age, they commonly develop degenerative valvular heart disease as well as degenerative diseases of other organ systems. In addition, a reservoir of patients with other forms of valvular heart disease develop progressive symptomatology with advancing age. These patients often present a challenge to the cardiologist in both diagnosis and management. Inasmuch as these patients tolerate cardiovascular surgery less well than their younger counterparts, criteria for surgical intervention may often need modification. Chronologic age must be recognized as but one of many factors affecting physiologic function. Knowledge of aging-related alterations in function must be employed in both diagnostic and therapeutic algorithms. At times, input from other health-care providers who specialize in the care of the elderly may assist in the assessment of these patients. Surgery should be reserved for higher-risk patients who are severely symptomatic or for those in whom severe symptoms are likely to soon develop based on the natural history of the disease process involved. Those less symptomatic elderly patients with otherwise preserved physiologic functions also may be offered valvular surgery. The availability of nonsurgical, albeit at times palliative, techniques to relieve aortic or mitral stenosis provides an alternative therapeutic option to cardiothoracic surgery. Advances in understanding the pathophysiology and medical therapy of heart failure will continue to contribute to an improved quality of life for those for whom only medical options exist.
Patients with heart failure frequently exhibit an excessive ventilatory response to exercise, which is acutely unaltered by therapeutic interventions. To investigate whether these ventilatory responses resolve after cardiac transplantation, 15 ambulatory patients with severe heart failure underwent exercise testing with measurement of respiratory gases before and 1.4 +/- 0.6 years [corrected] after transplantation. Ventilatory response was also measured in 7 age-matched, sedentary control subjects. Left ventricular ejection fraction at rest and hemodynamic measurements were obtained before and after transplantation in all patients. After transplantation, ejection fraction at rest increased from 16 +/- 6 to 56 +/- 10%, pulmonary capillary wedge pressure declined from 26 +/- 8 to 12 +/- 5 mm Hg, and cardiac index increased from 1.7 +/- 0.5 to 2.8 +/- 0.5 liters/min/m2 (all p less than 0.001). Peak oxygen consumption increased from 11.8 +/- 1.9 to 19.2 +/- 3.1 ml/kg/min (p less than 0.001), but remained significantly lower than that in control subjects (33.4 +/- 6.9 ml/kg/min; p less than 0.01). Minute ventilation (VE) was significantly reduced after transplantation, but excessive compared with normal values. Ventilation at a carbon dioxide production of 1 liter/min decreased significantly after cardiac transplantation (52.1 +/- 7.9 to 38.8 +/- 3.8 liters; p less than 0.01), but remained elevated when contrasted to that in control subjects (31.4 +/- 3.4 liters; p less than 0.05). Ventilatory response to exercise is significantly improved after cardiac transplantation; however, VE remains excessive. This may reflect an attenuated cardiac output response to exercise, abnormal intrapulmonary pressures or persistent deconditioning.
Changes in the beta-adrenergic receptor-G protein-adenylate cyclase complex were investigated in an experimental canine model of low-output heart failure produced by chronic rapid ventricular pacing. The contractile response occurring after exposure to the beta-adrenergic agonist dobutamine, measured as peak left ventricular + dP/dt, was decreased after 3 weeks of pacing. To further characterize the diminished functional responsiveness to beta-adrenergic receptor stimulation, beta-adrenergic receptor-adenylate cyclase coupling was investigated using membranes prepared from both control and paced animals. The density of beta-adrenergic receptors was decreased by 40% with a selective downregulation of the beta 1-subtype. The affinity of the receptor for the antagonist radioligand [125I]iodocyanopindolol remained unchanged. A defect in coupling was suggested by a decreased ability of isoproterenol, fluoride, and forskolin to stimulate adenylate cyclase in membranes prepared from failing hearts. Determination of the levels of Gi alpha (the alpha-subunit of Gi) by immunoblotting and pertussis toxin labeling revealed modest increases of approximately 30%. Furthermore, Mn2+ and purified Gs failed to stimulate adenylate cyclase in membranes prepared from failing hearts, indicating an impairment in the catalytic moiety of adenylate cyclase itself or in the ability of adenylate cyclase to couple to Gs. In contrast, complementation assay did not reveal differences in the functional activity of Gs alpha (the alpha-subunit of Gs). Taken together, these data demonstrate a selective decrease in the beta 1-subtype of adrenergic receptors and an increase in a 40-kd G1-like protein in the failing heart. Similar changes have been described in human idiopathic dilated cardiomyopathy. In addition to these changes, we identified a possible defect at the level of the catalytic subunit of adenylate cyclase.