Cystic adventitial disease of the popliteal artery: diagnosis and treatment.

PURPOSE: This paper represents the presentation of a case of cystic adventitial disease of the popliteal artery and an exhaustive review of the literature with an emphasis on optimal means for diagnosis and treatment of this unusual disease. METHODS: We collect all reported cases of cystic adventitial disease of the popliteal artery since the last review in 1987 with an additional review of these cases reported in the U.S. since the initial description of the disease. RESULTS: We found 264 cases of cystic adventitial disease (CAD) of the popliteal artery from 1954 to 1995, with 38 reported in the U.S. Fifty-eight new cases of CAD have been reported since the last review in 1987; 11 of these were reported in the U.S. Diagnosis of the disease has improved in the last few years with non-invasive techniques. Duplex color scanning followed by T2-weighted MRI now appears to be the best diagnostic choice. Various therapeutic methods have been described for the treatment of CAD. The recommended treatments are excision of the cyst with the cystic wall when the artery is stenotic and resection of the affected artery, followed by an interposition graft, when the artery is occluded. CONCLUSION: Claudication in young, healthy patients resulting from popliteal artery stenosis or occlusion is a leading symptom of CAD. This disease affects males in a ratio of approximately 5:1 and appears predominantly in the fourth and fifth decades. The incidence is approximately 1 in 1200 cases of claudication or 1 in 1000 peripheral arteriograms. The predominance of reported cases is found in Japan and Europe. Optimal diagnostic techniques include duplex color scanning and T2-weighted MRI. The lesions can be effectively treated by resectional or non-resectional means depending on the presence or absence of complete arterial occlusion.

Cardiovascular response to acute and chronic endotoxemia in an awake, volume-resuscitated, canine model.

The cardiovascular response to endotoxemia was evaluated in an awake, intravascular volume-resuscitated canine model. The animals were chronically instrumented for ultrasonic crystal dimension analysis and pressure measurements of the left ventricle (LV), aorta, right atrium (RA), and pulmonary artery (PA) and for cardiac output (CO) measurement. Lipopolysaccharide (Escherichia coli 011:B4) (LPS) was administered intravenously either as an acute, high dose bolus (5 mg/kg; n = 5), a high dose bolus after complete beta-blockade with propranolol (n = 3), or a chronic, low dose infusion (5 micrograms/kg/h; n = 7). Relative to baseline values, cardiac contractility was increased after acute high dose LPS bolus, however this effect was negated by beta-blockade. Chronic, low dose LPS infusion produced an increase in cardiac contractility at 1 h, a return to baseline by 4 h, and maximal contractile depression by 24 h. No change was seen in LV compliance after the high dose LPS bolus. The LV end diastolic volume was decreased by the high dose LPS bolus. This change was blocked by propranolol administration. Chronic LPS administration was accompanied by a decrease in LV compliance and an increase in LV end diastolic volume. Other cardiovascular indices (heart rate, CO, systemic vascular resistance) changed in a fashion similar to human sepsis. These findings confirm that endotoxemia in conscious canine subjects causes changes in cardiovascular function similar to that seen in human and animal models of sepsis. This study also allows us to explain some of the discrepancies between earlier studies of human sepsis and animal models in which the appropriate clinical conditions and an intact neuro-endocrine axis were not maintained.

Use of a modified van der Pol's oscillator to construct ventricular pressure-volume relations.

Ventricular pressure-volume (PV) loops provide information about ventricular function. Methodologic constraints have limited derivation of PV loops to the laboratory. The present study addresses derivation of PV loops from a direct left ventricular pressure measurement and left ventricular volume derived from continuous cardiac output. The measurements were performed in vivo in intact, innervated, normal canine hearts. Data from a total of 5 dogs and 13 different cardiac work states were analyzed. A nonlinear oscillator, a van der Pol's oscillator, described the PV relationships. Comparison of left ventricular stroke work derived from the van der Pol's oscillator model with that obtained from ultrasound transducers sutured directly to the myocardium demonstrated a linear correlation, close to the identity line, with R2 = 0.90. Modelling of LV PV loops by this technique was similar to loops derived by experimental measurements. This technique could lead to increased clinical uses for PV relationships.