Unproven Therapy Research Articles

Alternative and complementary cancer therapies

Alternative and complementary cancer therapies

Latissimus Dorsi Dynamic Cardiomyoplasty: Role of Combined ICD Implantation

Latissimus dorsi cardiomyoplasty is a promising surgical therapy in some patients with congestive heart failure. Although the mortality in heart failure patients is attributable primarily to heart failure and ventricular arrhythmias, the mechanism of death after cardiomyoplasty is not well characterized. We describe the clinical course of a patient undergoing cardiomyoplasty and discuss the role of combined use with an implantable cardioverter defibrillator. A 39-year-old man with congestive heart failure due to a massive anterior wall myocardial infarction was evaluated for latissimus dorsi cardiomyoplasty. The patient was in NYHA Functional Class III due to heart failure. He did not have any significant exertional or rest angina. During a Naughton stress test, the patient could exercise for 10 minutes, achieving 4 METS. Pulmonary function study showed a peak V O2 of 22.1 mL/min per kg. Radionuclide angiography demonstrated that the anterior wall was akinetic with a left ventricular ejection fraction of 22%. Cardiac hemodynamic studies suggested moderate pulmonary hypertension, elevated wedge pressure, and suboptimal response to exercise. A Holter recording showed frequent ventricular extrasystoles. Cardiomyoplasty was preferred to heart transplantation because the patient did not have end-stage heart failure. Postoperatively, the patient required low doses of dopamine. He developed recurrent, sustained, and hemodynamically significant episodes of ventricular tachycardia. He was treated with a combination of amiodarone and procainamide. He died 2 days postoperatively with ventricular fibrillation. Ventricular arrhythmias are a major cause of death in patients with heart failure. Latissimus dorsi cardiomyoplasty appears to be a promising but unproven therapy in such patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Dietary Recommendations to Prevent Coronary Heart Disease

The evidence that limiting dietary saturated fat and cholesterol will lower LDL cholesterol and contribute to the reduction in risk of cardiovascular disease is adequate for sound dietary recommendations to patients and to the public at large. Reduction of intake of all saturated fats to less than 10% of calories is a practical and achievable goal for Western man. Further reduction to less than 7% of calories is possible with a motivated and well instructed patient. The mechanism by which saturated fatty acids, particularly palmitate and laurate raise LDL cholesterol need detailed biochemical and physiologic study. Dietary cholesterol is unnecessary and clearly contributes to vascular disease in Western man. This vascular effect appears to be only partially explained by its effect on LDL cholesterol. Reduction to less than 300 mg per day for men of average size is achievable. Women and those eating fewer calories should strive for even less. Monounsaturated fats (oleic acid) can be consumed at levels of 20% of calories without significant concern if total calories are within limits to maintain desirable weight. Omega-6 polyunsaturated fats do not offer a significant health concern and need not be limited below the current intake of 7% of calories in the United States. Populations eating higher levels should be monitored to determine if such intakes are associated with either improved health or long-term ill effects since this level of intake has not been a long-standing tradition in any known culture. Omega-3 fatty acids might be increased to 2 or 3% of calories with potential benefit. Eating fish and marine animals is the most clearly documented safe method for achieving this. Larger intakes and particularly the use of fish oil supplements is unproven therapy for vascular disease prevention and needs much further study as a medical treatment for a variety of disorders. Protein intake is more than adequate in the USA and further increases could have negative effects on the prevalence of renal disease and osteoporosis. Although these issues are of hypothetical interest at the moment, they are worthy of considerable investigation. Complex carbohydrates consumed as components of vegetables, fruits and grains should be considered proven safe and healthful. Increasing calories from these sources at the expense of saturated fats and simple sugars should prove highly beneficial to Western populations. Fiber from these sources may have beneficial effects on blood cholesterol and intestinal function. Soluble fiber is documented to lower LDL cholesterol but the mechanism of this effect is not established and is worthy of considerable study.(ABSTRACT TRUNCATED AT 400 WORDS)

Historical Aspects of Hyperthermia in Cancer Therapy

The use of hyperthermia in cancer therapy had its origin in antiquity. Recently, some have hailed hyperthermia as the new fourth method of cancer therapy, and others have branded the treatment as "quackery" surrounded by mysticism, ignorance, and confusion. The American Cancer Society has been ambivalent, first placing it on its infamous unproven cancer therapy methods list, along with Laetril, Hoxey's cancer pills, hot water enemas, snake root oil, and other various and sundry "cancer cures." A few years ago the Society removed it from its list after deciding that hyperthermia may indeed have a place in future cancer therapy. This brief historical review highlights some of the most important early clinical discoveries and basic laboratory studies, which should help convince even the most avid skeptics of hyperthermia of the necessity of continuing the study of this most controversial form of cancer therapy.

Lack of objective improvement in ventricular systolic function in patients with myocarditis treated with azathioprine and prednisone

Six patients with myocarditis documented by biopsy, after a baseline right heart catheterization and echocardiogram, underwent treatment with azathioprine and prednisone. After 3 months of treatment, biopsy, right heart catheterization and echocardiogram were repeated. In addition to the immunosuppressive therapy, most patients received additional conventional medications for heart failure between evaluation periods (mean number of cardiac drugs increased from 1.7 +/- 1.0 to 2.7 +/- 0.05, p = 0.041). Mean heart rate decreased (105 +/- 14 to 84 +/- 13 beats/min, p = 0.016), as did pulmonary wedge pressure (23 +/- 8 to 12 +/- 4 mm Hg, p = 0.012). There were no significant changes in cardiac index (3.1 +/- 0.8 to 2.9 +/- 1.0 liters/min), end-diastolic dimension (62 +/- 13 to 62 +/- 12 mm) or fractional shortening (11 +/- 6 to 12 +/- 3%) with treatment. Complications from immunosuppressive therapy included severe soft tissue infection, acute psychosis and adrenal insufficiency in one patient each. The benefits from prednisone and azathioprine in this group of patients have not been demonstrated. Although heart rate and pulmonary wedge pressure decreased, these changes could be ascribed to increases in the conventional therapy for heart failure. Finally, there is a high incidence of side effects from prednisone and azathioprine therapy. These findings suggest that this unproven therapy for myocarditis should be limited to experimental protocols.

Idiopathic crescentic glomerulonephritis

Abstract There are three immunopathological mechanisms which account for the glomerular damage in the idiopathic crescentic GN syndrome. Type I patients have glomerular deposits of anti-GBM antibodies. Type II patients have immunohistologic evidence of immune aggregates along the glomerular basement membrane; type III patients have little or no immunoglobulin or complement deposition in the glomerulus. In all patients there is profound evidence of crescent formation. The pathogenesis of the glomerular crescent appears to involve the deposition of fibrin within Bowman's space and the migration of macrophages from the circulation into the area of fibrin deposition. The macrophage appears to be the cell which is central to the development of the lesion, although there is evidence that parietal epithelial cell proliferation also occurs. Recent experimental evidence has emphasized the role of the monocyte, not only in the generation of glomerular crescents, but also in the inflammatory reaction taking place in the glomerulus. These experimental data have raised the question of whether glomerular damage, particularly in the type III crescentic GN, may be the result of a pathogenetic process mediated by sensitized lymphocytes, rather than the classic humoral mechanisms. Irrespective of the pathogenetic mechanism, the ultimate concern of the clinician today is the effective therapy of the lesion, however empiric that therapy might be. Uncontrolled studies have supported approaches such as the use of anti-coagulants and antithrombotic agents, intravenous doses of massive amounts of methylprednisolone, and plasmapheresis therapy. The unfortunate clinician who must determine whether to use one or another unproven therapy with the attendant adverse side effects or accept the nihilistic approach of observing the natural course of this grim syndrome is left with a difficult decision. As there is little established data on which to base one's judgment, this decision must be made on a case-by-case basis and involves great caution and excellent therapeutic judgement. It has been said that clinical trials for the evaluation of treatment of various forms of crescentic GN are impossible because of the requirement for a cooperative multiple-clinic study and cumbersome investigative techniques. However, given the hint that certain of the uncontrolled observations of the effectiveness of therapy are valid and deserve substantiation, it seems inappropriate to continue to avoid the establishment of these studies. Surely, a great deal more money and manpower has been spent in biomedical research directed at more trivial problems. The establishment of clinical trials in this area is required if we are ever to approach the management of these patients rationally.