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Degenerative joint disease: cartilage or vascular disease?

The aetiology of degenerative joint disease is multifactorial, but one main cause is overloading (mechanical stress). While until recently it was well accepted that this represented primarily a disorder of cartilage with reactive subchondral changes, there is now some evidence that it might be primarily a subchondral problem with secondary changes in the articular cartilage. Early subchondral changes include redistribution of blood supply with marrow hypertension, oedema and probably micro-necrosis. These findings are very similar to those in avascular necrosis of bone and raise the question of a vascular aetiology. While these first reports need further proof, it seems clear that the articular cartilage and subchondral regions are one functional unit, in which the subchondral region is more stress sensitive. Recently described channels connecting these two regions strengthen this opinion. These new concepts are exciting and may make a major impact in the near future on the management of and research into degenerative joint disease.

Bone and Bones↗

Gene therapy for vascular diseases.

Arterial injury induces the synthesis of gene products that stimulate smooth muscle cell (SMC) migration and proliferation, leading to intimal hyperplasia. This process contributes to the pathogenesis of many cardiovascular diseases, including vascular proliferative diseases and atherosclerosis. Molecular approaches to the inhibition of SMC proliferation could potentially limit intimal expansion following vascular injury. During the past five years, there has been considerable interest in developing methods for the introduction and expression of recombinant genes in the vasculature. Gene transfer offers novel approaches to the study and treatment of vascular diseases. To date, gene transfer to the vasculature has been employed largely for two purposes: (1) examination of the expression and function of recombinant genes in vivo; and (2) development of potential new therapies for vascular diseases.

Animals↗

MRI of non-ischemic vascular disease: aneurysms and vascular malformations.

Due to flow-void phenomena, MRI is of great value in the demonstration of cerebral aneurysms and vascular malformations as well as of related parenchymal changes and hemorrhagic complications. Magnetic resonance angiography can produce vascular images which are of importance in the diagnosis and follow-up of the lesions.

Brain↗

Renal vascular disease causing end-stage renal disease, incidence, clinical correlates, and outcomes: a 20-year clinical experience.

In the United States, the incidence of end-stage renal disease to hypertension has increased sharply over the last 8 years, especially in elderly white dialysis patients who demonstrate very poor survival rates. The 5-year survival rates were near 20% for patients 65 to 74 years old and 9% for those > or = 75 years of age. Our program experienced a sharp increase in cases of end-stage renal disease due to renal vascular disease after 1982. Renal vascular disease was characterized clinically in 83 of 683 dialysis patients either by angiography or asymmetric kidney size in patients with evidence of systemic atherosclerosis, hypertension, insignificant proteinuria, and a benign urinary sediment. The median age was 70 years, with 84% of the patients being older than 61 years. These patients had 56% 2-year, 18% 5-year, and 5% 10-year survival rates, which are quite similar to the 1992 US Renal Data System data. Patients with renal vascular disease have a significantly worse prognosis than other diagnostic groups, most likely due to their older age, underlying vascular disease, and coronary artery disease. We feel that a significant number of elderly white hypertensive patients described in the 1992 US Renal Data Service report have renal vascular disease as a cause of end-stage renal disease, highlighting the need to establish correct renal diagnoses. Hypertension should not be the end-stage renal disease diagnosis in elderly white hypertensive patients if clinical criteria suggest a diagnosis of renal vascular disease.

Adult↗

Disease-based assessment of peripheral vascular disease in nursing facility patients.

OBJECTIVE: To determine the frequency of diagnosis of peripheral vascular disease (PVD) and selected related conditions in patients in a nursing facility, to determine the frequency of patients with risk factor(s) for or clinical evidence of PVD but without a diagnosis of PVD or a related condition, and to determine the frequency with which patients with and without a diagnosis of PVD or a related condition were treated with drug and nondrug therapies. DESIGN: A multicenter, disease-based, retrospective evaluation. SETTING: 41 nursing facilities in 6 regions of the US. PATIENTS: 4038 patients in a nursing facility: 827 patients with a PVD or related diagnosis; 2719 patients without a PVD or related diagnosis but with risk factor(s) for or clinical evidence of PVD; and 492 patients without a PVD or related diagnosis, risk factor(s), and clinical evidence. MAIN OUTCOME MEASURES: Evidence of disease and drug therapy for PVD. RESULTS: PVD was documented in 21% of patients; another 67% had risk factor(s) for or clinical evidence of PVD but no diagnosis of PVD or a related condition. Pentoxifylline was prescribed for 3% of the total sample and 12% of patients with PVD or a related condition. CONCLUSIONS: PVD appears to be inadequately evaluated in patients in a nursing facility. Disease treatment strategies should be developed and implemented to educate healthcare professionals and the general public about the need to acknowledge, assess, and treat PVD and related conditions.

Adult↗

Vascular diseases and oral infections.

Vascular diseases are multifactorial, and several risk factors, such as increasing age, male sex, hypertension, diabetes, dyslipidemias and smoking, are well-known. In recent studies, associations have also been found between preceding infections and development of myocardial or cerebral infarction. Preceding acute respiratory infections are reported to be more common in patients with myocardial or cerebral infarction. Cerebral infarction may follow infective endocarditis, bacterial meningitis or any other bacteremic infection. Oral infections are common chronic bacterial infections. Although oral infections are local, they may lead to systemic infectious complications via stransient bacteremias, and there may also be other systemic effects, for instance, via immunologic or toxic mechanisms. Association between oral infections and vascular diseases has been studied in 2 Finnish case-control studies concerning myocardial and cerebral infarction. In these case-control studies, it was found that oral infections were more common in patients with myocardial or cerebral infarction than in their age- and sex-matched community controls. There are many factors, such as diabetes, smoking and alcohol abuse, which may predispose to both development of infarction and oral infections. Therefore, the observed association between oral infections and vascular diseases may result from these common predisposing factors, and causality between them cannot be inferred. There are, however, several possible links between oral infections and infarction. Although causality between oral infections and infarction cannot be proven, patients who have poor oral health need health education, paying attention to those common risk factors of oral infections and vascular diseases. Furthermore, their oral infections should be treated, because they may predispose to infectious complications, which may lead to infarction.

Bacterial Infections↗

Arm exercise testing for coronary artery disease in patients with peripheral vascular disease.

We evaluated 74 peripheral vascular disease (PVD) patients (54 men, age 61 +/- 7 years and 17 women, age 63 +/- 7 years) for potential coronary heart disease (CAD) using an arm exercise test (AET) protocol. All patients performed upright two-arm cranking using discontinuous stages of 2 minutes of exercise separated by 2 minutes of rest. Exercise intensity was increased by +100 or 200 kpm (kilopond meters) with each stage. ECG was monitored continuously and blood pressure and 12-lead ECG tracings were obtained at the end of each exercise stage. All patients reached an endpoint of subjective exhaustion. Men achieved 91 +/- 14% of age-predicted heart rate at 597 +/- 167 kpm, while women achieved 86 +/- 14% of age-predicted heart rate at 335 +/- 117 kpm. Ischemic ECG responses (+AET) defined as new or additional ST depression greater than 1.0 mm X 80 ms, occurred in 35 men (65%) and 7 women (42%). Coronary angiography was performed in a subset of 22 patients (15 males and 7 females). CAD (greater than 70% stenosis) was found in 11 of 12 men and 4 of 5 women who showed positive or strongly positive AET responses (overall predictive value for AET = 88%). We conclude that arm exercise stress testing is safely performed in PVD patients who cannot complete treadmill exercise. In this limited series of PVD patients, the predictive value of a +AET response for diagnosis of CAD is similar to established values for treadmill exercise.

Adrenergic beta-Antagonists↗