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Biomedical subjects

M A Ricci

Publications and source records attributed to M A Ricci.

At least 37 records · Page 2Linked to original sources
PubMed1996

Effects of hypertension and propranolol upon aneurysm expansion in the Anidjar/Dobrin aneurysm model.

Propranolol has been suggested to slow aortic aneurysm (AAA) expansion by a mechanism independent of simple blood pressure (BP) reduction. To investigate this hypothesis, we designed a series of experiments to examine the effects of hypertension and propranolol upon AAA expansion. Using an established animal model, we induced AAA in normotensive and genetically hypertensive rats by perfusion of the isolated infrarenal aorta with elastase for two hours. Systolic tail BP was monitored with a plethysmograph. AAA size was measured directly with a micrometer on postoperative days 7 and 14. All data are expressed as the mean +/- standard deviation (SD). BP (mmHg) was significantly higher in hypertensive rats: 164 +/- 15 versus 119 +/- 7 (p < 0.001). AAA were also significantly larger in hypertensive rats with a mean expansion rate (mm/day) nearly twice that of normotensive animals: 0.13 +/- 0.09 versus 0.07 +/- 0.03. In a second series of animals, propranolol treatment was compared to placebo. In those animals, hypertensive propranolol-treated rats had significantly smaller AAA than placebo-treated controls (p < 0.05). There was no difference in normotensive animals but these rats had an unexplained paradoxical rise in BP with treatment. In this model, hypertension increases the expansion rate of AAA. Propranolol reduced the size of AAA in hypertensive animals, at least in part because of a decrease in BP. Other possible mechanisms of propranolol's action may be operative and require further study.

Adrenergic beta-Antagonists↗
PubMed1996

Hemodynamic and biochemical characteristics of the aorta in the WKY, SHR, WKHT, and WKHA rat strains.

This study was designed to characterize the hemodynamic and biochemical properties of the abdominal aorta in four genetically related inbred rat strains that express genetic hypertension and hyperactive behavior in varying combinations. These include (1) the spontaneously hypertensive rat (SHR), which is hypertensive, hyperactive, and hyperreactive to stress; (2) Wistar-Kyoto (WKY) rats, which express none of these traits; (3) WKHT rats, which are hypertensive but not hyperactive; and (4) WKHA rats, which are hyperactive and hyperreactive to stress, but normotensive. Together, these four strains allowed us to examine the structural and functional changes in the aorta in the hypertensive SHR, the most widely used animal model of genetic hypertension, while controlling for the variables of hyperactivity and hyperreactivity that are also expressed in the SHR. Four groups of animals of both sexes were studied: (1) WKY, n = 101, (2) WKHA, n = 33, (3) WKHT, n = 91, and (4) SHR, n = 28. Blood pressure (BP) was determined by tail plethysmography as well as direct intraarterial monitoring under anesthesia. Fixed specimens were prepared for histologic analysis and the wall thickness determined morphometrically. Quantification of soluble tissue protein, elastin, and collagen in the aortic tissue was determined by measuring leucine (leu), hydroxyproline (HP/leu), and desmosine (DES/leu). The hypertensive strains (SHR and WKHT) had significantly higher tail BP than the normotensive strains (WKY and WKHA)-WKY: 128.7 +/- 22.3; WKHA: 126.7 +/- 14.6; WKHT: 162.8 +/- 21.2; SHR: 164.2 +/- 36.1 (p < 0.0001). Additionally, intraaortic diastolic BP and mean BP were higher in SHR rats than in WKHT. Morphometric studies showed the media thickness in the SHR rats was significantly greater than in the WKY and WKHA rats and no different than in the WKHT rats. Significantly less of the aortic wall protein was present as elastin in the hypertensive rats (SHR and WKHT), as well as the hyperactive rats (WKHA), compared to rats that had neither trait (WKY). These studies provide new information regarding aortic structure and function in genetic hypertension using inbred strains to control for the hyperactivity/hyperreactivity traits that coexist with hypertension in the SHR. They reveal that hypertensive aortas have altered matrix proteins that cannot be explained simply on the basis of blood pressure alone.

Amino Acids↗
PubMed1996

The effect of peripheral vascular disease on long-term mortality after coronary artery bypass surgery. Northern New England Cardiovascular Disease Study Group.

OBJECTIVE: To examine the effect of peripheral vascular disease (PVD) on long-term mortality after successful myocardial revascularization. METHODS: We performed a regional cohort study of 2871 consecutive patients discharged alive after coronary artery bypass graft surgery at five tertiary care centers in Maine, New Hampshire, and Vermont between 1987 and 1989. Data reflecting patient characteristics, heart disease severity, and comorbidity were collected prospectively; the presence of clinical and subclinical indicators of PVD was determined by medical record review; and vital status was determined using the National Death Index (mean follow-up, 4.4 years). RESULTS: Five-year mortality following coronary artery bypass graft surgery was substantially higher in the 755 patients with indicators of PVD (20%; 95% confidence interval [CI], 17% to 23%) than in the 2116 patients without PVD (8%, 95% CI, 7 to 9; P<.001). The crude hazard ratio of long-term mortality associated with PVD was 2.77 (95% CI, 2.19 to 3.50; P<.001). After adjusting for their higher comorbidity scores, more advanced cardiac disease, and age, mortality rates in patients with PVD remained twice as high as those in patients without PVD (adjusted hazard ratio, 2.01; 95% CI, 1.57 to 2.58; P<.001). Long-term mortality was increased in patients with any of the indicators of PVD. Patients with multilevel PVD had especially high late mortality rates (adjusted hazard ratio, 2.46; 95% CI, 1.64 to 3.68; P<.001). CONCLUSIONS: Even after successful myocardial revascularization, patients with PVD remain at substantially increased risk for long-term mortality. The presence of clinical or subclinical PVD is important when predicting both short- and long-term outcomes in patients considering coronary artery bypass graft surgery.

Aged↗
PubMed1996

Anti-CD 18 monoclonal antibody slows experimental aortic aneurysm expansion.

PURPOSE: Inflammation has been implicated as a contributing factor in the expansion of abdominal aortic aneurysms (AAA). To test this hypothesis, we examined the effects of a monoclonal antibody (MAB) to the leukocyte CD18 adhesion molecule on the expansion of experimental AAA. METHODS: Aneurysms were induced by perfusion of an isolated segment of the infrarenal aorta with elastase in 22 normotensive (WKY) and 17 genetically hypertensive (WKHT) rats. Animals of both strains were randomly allocated to control or MAB-treated groups (MAB, 5 microgram/100 gm body weight intraperitoneally, daily, beginning on the operative day for a total of four doses). The activity of the MAB against rat leukocytes had first been determined by in vitro immunofluorescence flow cytometry. Aortic size was directly measured initially and on day 14. At that time, a segment of aorta was stained with hematoxylin and eosin and mononuclear leukocytes and neutrophils were counted in each of 10 microscopic fields (400X). RESULTS: The initial aortic size in all animals was 1.11+/-0.15 mm. All groups developed aneurysms significantly larger than the initial aortic size (p<0.01). However, the MAB-treated animals had significantly smaller aneurysms than the untreated controls (mm): WKY: 3.63+/-1.26, WKY-MAB: 2.08+/-0.30, WKHT: 4.54+/-1.86, WKHT-MAB: 2.37+/-0.40, p<0.0001. There also were significantly fewer monocytes in the MAB-treated normotensive rats: WKY:35.5+/-29.9, WKHT:40.6+/-28.8, WKY-MAB: 8.9+/-8.5, WKHT-MAB: 32.3+/-25.7, p=0.03. Neutrophil counts did not differ significantly between the groups. CONCLUSIONS: Treatment with anti-CD18 monoclonal antibody slows the expansion of AAA in this experimental model. The associated inflammatory process at day 14, as indicated by monocyte infiltration, is reduced, but this effect may be opposed by the presence of hypertension. Further evaluation of the role of leukocytes and adhesion molecules in the expansion of AAA is warranted.

Animals↗
PubMed1996

Practical equations to predict claudication pain distances from a graded treadmill test.

Treadmill testing is used to estimate the severity of claudication, but routine use is not practical or cost-effective in all settings. Thus, the purposes of this study were: (1) to develop and cross-validate prediction equations for treadmill claudication pain distances in a heterogeneous cohort of peripheral arterial occlusive disease patients, and (2) to determine if the regression equations were more accurate in assessing claudication distances than self-reported distances of patients. Medical history, vital signs, resting ankle/brachial systolic pressure index (ABI), and claudication distances during a graded treadmill test were obtained on a validation group of 178 claudicants and on a cross-validation group of 94 claudicants. The independent predictors of claudication pain distances of the validation group were ABI, body mass index, gender, and current smoking status, with multiple correlation coefficients of R = 0.73 and R = 0.82 for the distances to onset and to maximal pain, respectively. These equations were successfully cross-validated on an independent group of claudicants, as the predicted distances to onset of claudication pain (167.2 +/- 102.6 m) and to maximal pain (354.6 +/- 154.3 m) were similar (p = 0.99) to measured distances (169.1 +/- 127.8 m and 356.6 +/- 181.0 m, respectively). However, the self-reported distances to onset (89.5 +/- 126.3) and to maximal claudication pain (189.2 +/- 284.3) were 1-2 blocks less than either the measured or predicted distances (p < 0.01). It is concluded that claudication pain distances during an incremental treadmill test can be more accurately estimated from a composite of variables obtained during medical screening than by relying on the self-report of patients. Consequently, in clinical settings where treadmill testing is impractical, the functional severity of claudication can be assessed without exercise testing.

Aged↗
PubMed1995

Intravenous leiomyomatosis with intracardiac extension.

Intravenous leiomyomatosis is a benign smooth muscle tumor of uterine origin characterized by grossly visible masses of smooth muscle cells growing within venous channels. A case of leiomyomatosis arising in the uterine veins with extension into the right iliac veins, vena cava, right atrium, right ventricle and into the pulmonary outflow tract is described. The tumor was completely and successfully removed by a staged approach with median sternotomy followed by laparotomy several days later. A brief review of the literature and a discussion of the operative approach are presented.

Adult↗
PubMed1995

The effect of peripheral vascular disease on in-hospital mortality rates with coronary artery bypass surgery. Northern New England Cardiovascular Disease Study Group.

PURPOSE: The purpose of this study was to examine the effect of peripheral vascular disease (PVD) on in-hospital mortality rates after coronary artery bypass grafting (CABG). METHODS: We performed a regional cohort study of 3003 patients undergoing CABG between 1987 and 1989 at five tertiary care centers in Maine, New Hampshire, and Vermont. Data reflecting patient characteristics, severity of heart disease, comorbidity, and in-hospital mortality rates were collected prospectively; the presence of clinical and subclinical indicators of PVD was determined retrospectively. RESULTS: Observed in-hospital mortality rates with CABG were 2.4-fold higher in the 796 patients with indicators of PVD (7.7%) than in the 2207 patients without PVD (3.2%) (crude odds ratio [OR] 2.42 [95% confidence interval (CI) 1.73-3.37]). After adjusting for their higher comorbidity scores, more advanced heart disease, and age, patients with PVD remained 73% more likely to die in hospital after CABG (adjusted OR 1.73 [CI 1.19-2.51]). The excess risk of in-hospital death associated with PVD was attributable largely to lower extremity occlusive disease (adjusted OR 2.03 [CI 1.34-3.07]). Subclinical lower extremity occlusive disease (asymptomatic absence of pedal pulses) had the same effect as clinically overt disease. Cerebrovascular disease had a small and statistically nonsignificant effect on CABG-related deaths (adjusted OR 1.13 [CI 0.73-1.74]). Excess mortality rates in patients with PVD were primarily due to increased risk of death from heart failure and dysrhythmias, but not to cerebrovascular accidents or peripheral arterial complications. CONCLUSIONS: The presence of lower extremity arterial occlusive disease is an important, independent predictor of in-hospital mortality rates for patients undergoing CABG. Controlled studies of the long-term effects of CABG in patients with PVD are needed to determine the optimal role of myocardial revascularization in this population.

Aged↗
PubMed1995

Enhanced revascularisation after angiogenic stimulation in a rabbit model of bilateral limb ischaemia.

OBJECTIVE: We previously demonstrated stimulation of collateral vessel formation in a rabbit model of unilateral limb ischaemia after administration of endothelial cell growth factor (ECGF). To distinguish clearly the effects of ischaemia alone from those of ischaemia combined with angiogenic stimulation in the same animal, a model of bilateral hindlimb ischaemia was used to evaluate further the angiogenic effect of ECGF. DESIGN: Ischaemia was produced in both hindlimbs of 11 rabbits by femoral artery excision. Beginning 10 days later, ECGF (8 mg in 3 ml of saline) was injected in one hindlimb while 3 ml of saline alone was injected in the other every other day for a total of five doses. OUTCOME MEASURES: Calf systolic blood pressure was measured in both limbs on postoperative days, 10, 30, and 50. On day 50, collateral formation was quantitated angiographically, and muscle samples were obtained for quantitation of capillary density and histologic studies. RESULTS: The mean calf systolic blood pressure in the both hindlimbs was similar on day 10 (36.9 +/- 2.3 versus 38.1 +/- 2.9 mmHg) but was significantly higher in the ECGF-treated limb on day 30 (68.9 +/- 3.1 versus 45.0 +/- 2.9 mmHg) and day 50 (83.0 +/- 3.0 versus 57.0 +/- 1.7; p < 0.0001 for both comparisons). On day 50, collateral vessels were significantly more numerous in the ECGF-treated limb (17.2 +/- 1.6 versus 11.0 +/- 0.8; p < 0.0006), as were capillaries (225.9 +/- 11.4 versus 159.6 +/- 12.9 per mm2; p < 0.002). CONCLUSION: Local administration of ECGF enhanced collateral development leading to significantly improved perfusion in the treated as compared with the untreated limb in the same animal. Exogenous administration of an angiogenic mitogen can upregulate the normal collateral response to ischaemia and may be useful in treating severe limb ischaemia.

Angiography↗
PubMed1995

Routine prophylactic vena cava filter insertion in severely injured trauma patients decreases the incidence of pulmonary embolism.

BACKGROUND: Trauma patients are at increased risk for venous thromboembolism despite routine prophylaxis. A five-year retrospective review of pulmonary embolism at the Medical Center Hospital of Vermont showed that four types of injuries (head injuries, spinal cord injuries, complex pelvic fractures, and hip fractures) accounted for 92 percent of pulmonary emboli in patients on the trauma service. STUDY DESIGN: Beginning July 1991, all patients who met criteria for a high-risk injury (excluding hip fractures) had prophylactic vena cava filters inserted percutaneously in the radiology suite. Weekly impedance plethysmography was performed for the detection of deep vein thrombosis. Following discharge, abdominal duplex ultrasound was performed at one month, six months, and yearly to check filter position and patency. RESULTS: To date, a total of 63 patients, or 2 percent of the total trauma population, had prophylactic vena cava filters inserted. There were 19 (30 percent) deep vein thromboses in this population of patients and one patient had a pulmonary embolism (1.5 percent). Overall there was significant (chi-square, p < 0.00072) reduction of pulmonary embolism on the trauma service compared to the historical controls. Follow-up examination with abdominal duplex ultrasound showed a 30-day patency rate of 100 percent and a one- and two-year patency rate of 96.1 +/- 3.8 percent by life-table analysis. CONCLUSIONS: We concluded that prophylactic vena cava filters are efficacious in decreasing the risk of pulmonary embolism in high-risk trauma patients.

Adult↗
PubMed1994

Vascular complications of cardiac catheterization.

Peripheral vascular complications after cardiac catheterization constitute an increasing portion of traumatic vascular injuries. To determine the incidence of these complications and the sequelae of their treatment, we reviewed 7,690 catheterizations performed over a 40-month period. One hundred eleven vascular complications were detected (1%), 41 of which required surgical repair (0.5%). Pseudoaneurysm (10), arteriovenous fistula (4), thromboembolism (9), infection (5), and other bleeding complications (83) were all found. Significantly more complications occurred in patients who were older than 60 years of age or female (P < 0.0009). In addition, the likelihood of a vascular injury after coronary angioplasty was significantly higher than after angiography alone (3% versus 1%, P < 0.00001). Secondary local and systemic complications after surgical repair were more frequent compared with those injuries that were managed nonoperatively (32% versus 11%; P = 0.015). Vascular complications continue to be a significant problem after cardiac catheterization, especially when coronary angioplasty is performed. The sequelae of surgical repair are significant, adding to their morbidity. Periodic review of these complications may identify factors that might be modified to reduce complications.

Aneurysm, False↗
PubMed1994

Expansion of aortic aneurysms is reduced by propranolol in a hypertensive rat model.

PURPOSE: It has been suggested that propranolol has unique effects that slow aneurysm expansion by remodeling the structural proteins of the aorta. These effects are believed to be independent of blood pressure reduction, a hypothesis we tested in this investigation with a rat model of abdominal aortic aneurysm (AAA). METHODS: With an established model, AAA were induced in normotensive Wistar-Kyoto (WKY) rats and genetically hypertensive Wistar-Kyoto (WKHT) rats by perfusing an isolated segment of the infrarenal aorta with elastase. A propranolol dose-response was studied for each strain: (1) saline solution controls (n = 18); (2) propranolol, 10 mg/kg subcutaneously (n = 18); (3) propranolol, 30 mg/kg (n = 14). Systolic blood pressure was determined by tail plethysmography before operation and on day 14, as well as by direct recording at surgery and on day 14. Rats were killed at 14 days, and aneurysm diameter was measured. RESULTS: The initial tail BP was 129 +/- 22 mm Hg in WKY animals and 158 +/- 21 mm Hg in WKHT animals (p < 0.0001). Tail BP and intraaortic systolic, diastolic, and mean blood pressure (BP) were not significantly decreased by propranolol treatment in either strain of rats. However, BP tended to rise in WKY rats, whereas it fell slightly in WKHT rats. Initial aortic size in all animals was 1.06 +/- 0.12. The final aortic size in untreated, hypertensive rats was more than twice that of untreated normotensive controls: 1: WKHT, 3.0 +/- 0.73 mm, 1: WKY, 6.9 +/- 3.5 mm (p < 0.01). After treatment with both doses of propranolol, hypertensive aneurysms were significantly smaller than the untreated WKHT group (p < 0.05) and not significantly different from aneurysms in all groups of normotensive animals: 2: WKY, 3.1 +/- 1.13 mm, 2: WKHT, 4.0 +/- 1.81 mm; 3: WKY, 4.1 +/- 0.41 mm, 3: WKHT, 2.9 +/- 1.24 mm. There was no significant difference in aortic size between the three normotensive WKY groups. CONCLUSIONS: Hypertension increases the size of aortic aneurysms in this experimental model. Propranolol significantly reduces the size of experimental AAA in hypertensive animals independently of the dose and by a mechanism that may be unrelated to simple BP reduction.

Analysis of Variance↗
PubMed1994

Abdominal aortic aneurysm expansion rate: effect of size and beta-adrenergic blockade.

PURPOSE: The purpose of this study was to investigate the hypothesis that abdominal aortic aneurysm (AAA) expansion may be slowed by beta-adrenergic antagonists. METHODS: One hundred twenty-one patients with infrarenal AAA were monitored with serial aortic ultrasound examinations. Eighty-three patients received no beta-blockers (group I), and 38 patients received beta-blockers (group II). Values are expressed as mean +/- SD. RESULTS: The mean follow-up was 43 +/- 29 months with 5.5 +/- 3.4 ultrasound examinations per patient. The expansion rate among all AAA was 0.38 +/- 0.44 cm/yr. Large aneurysms (> or = 5 cm) expanded significantly faster than small aneurysms (p = 0.02) in patients not treated with beta-blockers. Among patients with large AAA, those receiving beta-blockers had a significantly reduced mean expansion rate; 0.36 +/- 0.20 versus 0.68 +/- 0.64 cm/yr, (p < 0.05). Although rupture rates were lower in group I (5%) versus group II (13%), this difference was not statistically significant. Thirty-four patients in a poor-risk category with AAA were monitored greater than 5 cm in diameter. Ten of these AAA ruptured. The mean expansion rate was significantly greater in those patients with ruptured AAA versus those patients with AAA that did not rupture; 0.82 +/- 0.74 versus 0.42 +/- 0.41 cm/yr (p = 0.04). CONCLUSIONS: In patients not undergoing beta-blocker therapy, large AAA expand at a significantly greater rate than smaller AAA. Large aneurysms that rupture show more rapid expansion than those AAA that do not rupture. We have demonstrated a significantly reduced rate of expansion of large AAA in patients receiving beta-blockade.

Adrenergic beta-Antagonists↗
PubMed1994

Prophylactic vena cava filter insertion in patients with traumatic spinal cord injury: preliminary results.

Pulmonary embolism (PE) is a devastating complication in patients with traumatic spinal cord injury (SCI). Prophylactic measures such as venous compression hose or low-dose heparin are only partially protective in reducing the risk of venous thromboembolism and are contraindicated in some patients. Because of extended perturbations in fibrinolytic activity, catecholamine effects on platelet aggregation, increased activity of complement and acute phase reactants, abnormally high factor VIII concentrations, and persistent venous stasis with ongoing endothelial damage, the patient with an SCI remains at prolonged risk for venous thromboembolism. A retrospective 5-year review at the Medical Center Hospital of Vermont revealed seven patients with eight documented PEs (three fatal; 2.7%) in 111 SCI patients (6.3%). Six PEs (75%) occurred after discharge from the acute care facility. Median time to PE after injury was 78 days (range, 9-5993). Although comprising only 4% of all trauma admissions, SCI accounted for 31% of all PEs in the total trauma population (2525 patients). Beginning in July 1991, a new prophylaxis protocol was instituted, which included the percutaneous insertion of vena cava filters under local anesthesia in all SCI patients with paraplegia or quadriplegia. Fifteen patients have undergone the insertion of titanium filters. Impedance plethysmography was performed weekly to detect deep venous thrombosis. No complications were associated with vena cava filter insertion. No patients developed deep venous thrombosis during their acute hospitalization (median, 22 d), and no patients have developed PE after filter insertion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

Hypertension accelerates the growth of experimental aortic aneurysms.

Hypertension has long been suspected to increase the growth rate of abdominal aortic aneurysms (AAA), but there is little experimental evidence to support this hypothesis. Using an established model, aneurysms were induced in normotensive Wistar-Kyoto (WKY) rats and in a unique strain of genetically hypertensive Wistar-Kyoto (WKHT) rats by perfusing an isolated segment of the infrarenal aorta with elastase (n = 14, each group). Aortic diameter was measured with a micrometer and systolic blood pressure (sBP) determined by tail plethysmography. Rats were killed at 7 or 14 days, aneurysm diameter was measured, and aneurysms were examined histologically. Systolic blood pressure was significantly higher in WKHT rats (164 +/- 15 mm Hg) compared to WKY animals (119 +/- 7 mm Hg, P < 0.001). Initial aortic size was 1.10 +/- 0.02 mm in the two groups. Aneurysms in the hypertensive animals were significantly larger at Day 7 (WKY, 2.31 +/- 0.09 mm; WKHT, 2.54 +/- 0.22 mm; P = 0.02) and Day 14 (WKY, 2.36 +/- 0.25; WKHT, 3.45 +/- 0.89; P = 0.001). Overall, the mean AAA growth rate of the WKYHT group was nearly twice that of the WKY group: 0.13 +/- 0.09 mm/day vs 0.07 +/- 0.03 mm/day, (P = 0.004). Growth rates were also positively correlated with sBP (r = 0.82, P < 0.0001). Both groups showed elastic lamellar disruption and inflammatory cell infiltration within the wall of the aorta. As demonstrated in this experimental model, hypertension does indeed increase the rate of growth of AAA.

Animals↗