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Using experimental models of various disease states, the ability of the isolated perfused working rat heart to withstand and recover from a period of severe ischemia was investigated. The results revealed that the coexistence of a diabetic state, obesity, or left ventricular hypertrophy increased the susceptibility of the hearts to ischemic damage and reduced the rate or the extent of postischemic recovery. In contrast, hearts obtained from moderately hypertensive rats exhibited a greater resistance to, and a superior recovery from, ischemia than did hearts obtained from normotensive controls.
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PMID:Myocardial susceptibility to ischemic damage: a comparative study of disease models in the rat. 15 26

Dysbaric osteonecrosis appears to be independent of decompression sickness. The 2 conditions, however, may share etiologic and pathogenetic factors. The incidence of osteonecrosis is influenced by the number of hyperbaric exposures, extent of pressure, decompression profile and possibly by the rate of compression and degree of obesity. Though etiology and pathogenesis are unclear, osteonecrosis is probably due to ischemia, with gas bubbles causing direct or indirect circulatory impairment. In vitro experiments, as well as human and animal studies, suggest multiple pathogenetic mechanisms: intraosseous vessel compression by extravascular bubbles; vessel obstruction by bubbles, fibrin thrombi, platelet aggregates, clumped erythrocytes or coalesced lipids; and narrowing of arterial lumina by bubble-induced myointimal thickening. Obstructing materials, whether autochthonous or embolic, may result from blood-bubble interface reactions. Rheologic changes and blood flow redistribution could play contributing roles. It seems likely that multiple pathogenetic factors act in concert or sequentially. Proposed nonischemic changes, such as hyperoxic injury gas-induced osmosis, or autoimmunity, lack sufficient supporting evidence. The peculiar vulnerability of bone may be related to gas supersaturation of the fatty marrow; sensitivity to extravascular gas pressure because of tissue rigidity; poor vascularization; and the presence of uranium 238 which promotes nucleation and subsequent gas bubble formation.
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PMID:Dysbaric osteonecrosis. Etiological and pathogenetic concepts. 63 12

Recent epidemiologic studies have suggested that cardiac disease in common in diabetics and may often have a noncoronary basis. To examine the status of the left ventricle, 17 adult-onset diabetics of familial type without hypertension or obesity underwent hemodynamic study and were compared to 9 controls of similar age. Of the 17, 12 subjects had no significant occlusive lesions by coronary angiography. From this group eight without heart failure had a modest, but significant, elevation of left ventricular end-diastolic pressure. End-diastolic and stroke volumes were reduced, but ejection fraction and mean rate of fiber shortening were within normal limits. The left ventricular end-diastolic pressure/volume ratio was significantly higher than controls. Afterload increments effected a significant increase of filling pressure compared to normals without a stroke volume response, consistent with a preclinical cardiomyopathy. Four patients with prior heart failure had similar but more extensive abnormalities. None had local dyskinesia by angiography, and lactate production was not observed during pacing-induced tachycardia. Left ventricular biopsy in two patients without ventricular decompensation showed interstitial collagen deposition with relatively normal muscle cells. These findings suggest a myopathic process without ischemia. Postmortem studies were performed in 11 uncomplicated diabetics. Nine were without significant obstructive disease of the proximal coronary arteries, and the majority succumbed with cardiac failure. On left ventricular sections, none had evident luminal narrowing of the intramural vessels. All nine exhibited periodic acid-Schiff-positive material in the interstitium. Collagen accumulation was present in perivascular loci, between myofibers, or as replacement fibrosis. Multiple samples of left ventricle and septum revealed enhanced triglyceride and cholesterol concentrations, as compared to controls. Thus, a diffuse extravascular abnormality may be a basis for cardiomyopathic features in diabetes.
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PMID:Evidence for cardiomyopathy in familial diabetes mellitus. 89 79

In a population of 744 diabetics composed mainly of elderly female patients, 172 developed hypertension after the onset of diabetes. Compared to normotensive diabetics, they had an increased prevalence of diabetic retinopathy (p less than 0.001), cerebral accidents, ischemic disorders of the lower limbs and a decreased glomerular filtration rate (p less than 0.05); they are frequently insulin-dependent and difficult to manage. In 173 other indivuals the diabetes emerged several years after the hypertension. This group was characterized by relatively easily controlled blood sugar and increased prevalence of angina and myocardial infarction (p less than 0.001). The association of hypercholesteremia with hypertension increases the risk of coronary disease (p less than 0.02) and, to a lesser degree, of glomerular insufficiency. The prevalence of coronary symptoms increases with obesity (p less than 0.05) while retinopathy increases with insulin dependence (p less than 0.001). From this information it may be concluded that the importance of various risk factors in the diabetic chiefly varies according to the vascular territory involved: cerebral vascular accidents occur mainly in hypertensives, while the presence of retinopathies, proteinuria and peripheral ischemia is directly related to the diabetes and particularly to insulin dependence. The risk of coronary lesions increases considerably when hypertension is added to the diabetes, with an even greater risk in the case of a diabetic, hypertensive, hypercholesterolemic nexus.
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PMID:[Factors of arterial and renal complications in diabetes]. 112 60

Coronary heart disease is the most frequent cause of death in Western, industrialized countries. Coronary risk factors are prevalent in such countries and sometimes combine to constitute the so-called syndrome X--hypertension, central obesity, serum lipid and clotting disturbances, and insulin resistance. beta-Blockers, unlike calcium antagonists, have proved highly effective in secondary prevention of myocardial infarction. If present at the time of the myocardial infarction, beta-blockers (unlike calcium antagonists and diuretics) probably decrease mortality 1 month later. Early intervention (within 12 h) of chest pain with intravenous beta-blockers results in a 15% reduction in cardiovascular mortality at 1 week. Later intervention (3-28 days) with oral non-ISA beta-blockers results in a 30% reduction in mortality after 1 year; ISA-containing beta-blockers are probably less effective (less decrease in heart rate). Hydrophilicity/lipophilicity of beta-blockers is unimportant in terms of decreased mortality. Primary prevention of myocardial infarction, unlike stroke, in hypertensive patients has been disappointing, possibly due to treatment-induced biochemical/lipid changes or inappropriate lowering of diastolic blood pressure in high-risk subjects (J-curve effect). beta-Blockers should be first-line therapy for hypertensive patients up to the age of 65 years, particularly men (and nonsmokers) as Q-wave myocardial infarction is significantly decreased by beta-blockers and significantly increased by diuretics. However, in elderly hypertensive subjects, beta-blockers have not significantly decreased myocardial infarction (unlike stroke), whereas diuretics have. The effects of beta-blockers and diuretics on heart size (and thus coronary flow reserve) in the elderly may be important. Thus, beta-blockers should be second-line therapy for the elderly hypertensive individual but first-line if overt ischemia (e.g., angina or recent myocardial infarction) also is present. In patients with angina but normal blood pressure, beta-blockers tend to decrease and calcium antagonists increase cardiovascular events. Thus, beta-blockers are highly effective agents in the secondary prevention of myocardial infarction and are moderately effective in primary prevention of myocardial infarction in hypertensive patients (particularly men) under the age of 65 years.
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PMID:Beta-blockers: primary and secondary prevention. 128 45

The author analyses distant results of the Polish vascular prostheses implantation to 227 patients with aorto-iliac occlusive disease. Eighty two (29.6%) patients died within 5 years following the operation. Therefore, an analysis of the distant results of therapy included 145 patients. An excellent result was achieved in 20.7% of the treated patients, satisfactory result in 53.9%, no improvement or worsening in 20.7% of cases. Statistically significant relationship between the degree of pre-operative ischemia and outcome of surgery has been noted. Considering blood hypertension, diabetes mellitus, obesity, hypercholesterolemia, and tobacco smoking prior to and after surgery as risk factors, no statistically significant relationship between the distant result of the treatment and the number of risk factor in a single patient has been observed.
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PMID:[Long-term results of aorto-iliac occlusive disease treatment with implantation of the Polish vascular prosthesis]. 140 58

The goal of cardiac rehabilitation is to optimize function through attention to the patient's medical needs, risk factors for recurrent events, physical reconditioning, and psycho-social needs. Medical needs include beta-adrenergic blocking agents and aspirin unless contraindicated, angiotensin converting inhibitors for left ventricular dysfunction, and relief of residual ischemia. Smoking, lipid abnormalities, physical inactivity, and hypertension remain important predictors of reinfarction and death and must be controlled. Obesity must be addressed because it exacerbates these problems. Therefore, the principles of behavior change should be applied to help patients control their risk factors and adopt healthy lifestyles. Smoking cessation and appropriate dietary behaviors can be adopted by the patient while in the hospital. Physical reconditioning can also begin with twice-daily exercises. After discharge from hospital and after an initial submaximal exercise evaluation, the patient will benefit from three sessions per week of outpatient cardiac rehabilitation for six to eight weeks. These sessions should last about an hour and raise the patient's heart rate as much as 30 beats per minute. Along with physical reconditioning, the cardiac rehabilitation program provides an opportunity to address risk factor modification, return to work, return to sexual activity, management of depression and anxiety, and the presence of risk factors in the patient's family. The patient should attend reinforcing sessions every three months for the first year and as necessary after that to control risk factors and reinforce the necessity for physical fitness.
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PMID:Cardiac rehabilitation 1992. 143 5

3 cases of popliteal artery occlusion are described, in 2 young Israeli women and a young man, and the etiologic factors in this rare disorder are reviewed. The 1st case was a 20-year old healthy woman with no contributing factors except use of low dose oral contraceptives for 5 months. She had suffered for 3 months with claudication of her left leg. Her Doppler ankle-brachial index was 0.7, and her angiogram showed complete occlusion of the popliteal artery and partial occlusion of the tibio-peroneal. She was treated with aspirin and cardoxine, discontinuation of oral contraceptives and walking, and recovered. The 2nd case was a 33-year old woman with history of rheumatic fever, obesity, hirsutism, venous thrombosis, hormone therapy for infertility, multiple spontaneous abortions, smoking, and possible Cushings disease. Her findings included and AB index of 0.45 on the right, and spotty stenosis of the popliteal artery. She was treated surgically with a Fogarty catheter, and is well 3 years later with the help of anticoagulants. The 3rd patient was a 30-year old male athlete who smoked heavily. He had an AB index of 0.4 on the left and complete blockage of the popliteal artery, so he received longitudinal arteriotomy and thrombectomy. He was put on anticoagulants, and is well, 6 months after surgery. Oral contraceptives were considered the likely cause of the 1st young woman's claudication, and possibly involved in the 2nd patient's ischemia. It is usually difficult to define the cause of isolated popliteal artery occlusion in young adults. Multidisciplinary management with thrombolytics or surgery should be considered, and discontinuation of oral contraceptives should be a priority, especially if a young woman began using them in the last year.
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PMID:Isolated popliteal artery occlusion in the young. 144 85

Atherosclerotic changes of carotid and lower extremity arteries were studied in the selected industrial population represented by 58 men with arterial hypertension. Affection of peripheral arterial system was detected by means of non-invasive ultrasound methods. Stenoses of carotid arteries were recorded in 19% of cases (11 of 58), stenoses of lower extremity arteries in 7% (4 of 58). Hypertonic individuals did not show neurological symptomatology, including one patients with total occlusion of the arteria carotis interna. One man underwent the attack of cerebrovascular ischemia. Stenoses of lower extremity arteries were also in the subclinical stage and without intermittent claudications. A high number of risk factors of atherosclerosis was found in the series: obesity in 90%, smoking 57%, hypercholesterolemia in 47%. Peripheral arterial changes were associated with combined risk factors (two and more). This indicates their involvement in the origin and development of atherosclerotic lesions.
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PMID:Carotid and lower extremity arterial disease in hypertensions. 183 75

Many clinical studies have shown an increased insulin response to oral glucose in patients with ischemia of the heart, lower limbs, or brain. Hyperinsulinemia also occurs in patients with angiographically proved atherosclerosis without ischemia and thus appears to be related to arterial disease and not to be a nonspecific response to tissue injury. Fasting insulin levels and insulin responses to intravenous stimuli, including glucose, tolbutamide, and arginine, are normal, suggesting a gastrointestinal factor may be involved in the increased insulin response to oral glucose. In patients with atherosclerosis, insulin sensitivity appears to be normal or enhanced with respect to both glucose and lipid metabolism. Five population studies have shown that insulin responses to glucose are higher in populations at greater risk of cardiovascular disease. Many of the hyperinsulinemic populations also had upper-body obesity, hypertriglyceridemia, lower high-density lipoprotein (HDL) levels, and hypertension. These prospective studies support an independent association between hyperinsulinemia and ischemic heart disease, although their results differ in detail. Hyperinsulinemia is associated with raised triglyceride and decreased HDL cholesterol levels. Total and low-density lipoprotein (LDL) cholesterol is less closely related to hyperinsulinemia. Upper-body adiposity is associated (in separate studies) with coronary heart disease, diabetes, hyperinsulinemia, and hypertriglyceridemia. Insulin and blood pressure are closely related in both normotensive and hypertensive people. Although obesity and diabetes are often found in hypertensive people, hyperinsulinemia also occurs in nonobese nondiabetic hypertensive people. Thus, hyperinsulinemia is closely associated with a cluster of cardiovascular risk factors, i.e., hypertriglyceridemia, low HDL levels, hypertension, hyperglycemia, and upper-body obesity. There is a possibility that insulin has a role in the sex differences in ischemic heart disease incidence and their absence in diabetes, but additional work is required for its clarification. Long-term treatment with insulin results in lipid-containing lesions and thickening of the arterial wall in experimental animals. Insulin also inhibits regression of diet-induced experimental atherosclerosis, and insulin deficiency inhibits the development of arterial lesions. Insulin stimulates lipid synthesis in arterial tissue; the effect of insulin is influenced by hemodynamic factors and may be localized to certain parts of the artery. In physiological concentrations, insulin stimulates proliferation and migration of cultured arterial smooth muscle cells but has no effort on endothelial cells cultured from large vessels. Insulin also stimulates cholesterol synthesis and LDL binding in both arterial smooth muscle cells and monocyte macrophages.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Insulin and atheroma. 20-yr perspective. 199 42


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