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Background: Recent limitations in Medicaid coverage of transplantation in Arizona jeopardized transplantation of potential recipients in that state and called attention to financial barriers inherent in the present organ allocation system. Policies of cardiac transplant centers regarding insurance requirements for transplantation have not been previously assessed. We sought to determine the policies of adult cardiac transplant programs nationwide regarding insurance requirements for evaluation and listing for cardiac transplantation., Methods: From December 15, 2008 to November 16, 2010, all active adult cardiac transplant programs in the United States were surveyed regarding insurance requirements for evaluation and listing for cardiac transplantation., Results: Surveys were completed by 62 of 101 programs, accounting for 71% of adult cardiac transplants in 2007. Only 2% of recipients were uninsured. Insurance was required by 48% of programs to evaluate and 84% to list for transplantation. For uninsured patients, 81% of programs required a large amount of money upfront (median, $200,000; interquartile range, $10,000-$300,000) to list for transplantation and often (84%) educated patients about fundraising to acquire these resources., Conclusions: Adult cardiac transplant programs generally require candidates to have adequate health insurance to undergo transplantation. Uninsured patients typically need a significant amount of money upfront to be listed for transplantation and often are advised to fundraise to gather such resources., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Objective: The objective of our study was to evaluate the safety of CO(2) and gadodiamide angiography for diagnosing and percutaneously treating renal artery stenosis in patients with chronic renal insufficiency and presumed ischemic nephropathy., Subjects and Methods: One hundred forty-six consecutive patients with chronic renal insufficiency (serum creatinine > 1.5 mg/dL) were examined for renal artery stenosis using CO(2) and gadodiamide as the angiographic contrast agents. If renal artery stenosis was detected, percutaneous balloon angioplasty with or without stenting was performed. In patients for whom 48-hr creatinine levels were available, we performed an analysis to determine the incidence of contrast-involved nephropathy (increase in serum creatinine of 0.5 mg/dL at 48 hr without identifiable cause). Major complications were reported up to 1 week, and mortality was reported up to 30 days after the procedure., Results: Ninety-five patients had serum creatinine levels available at 48 hr. An increase in creatinine of greater than 0.5 mg/dL at 48 hr occurred in three patients (3.2%), presumably caused by CO(2), by gadodiamide, or by both. Neither diabetes nor the degree of preexisting chronic renal insufficiency was a predictor of worsening renal function 48 hr after the procedure. The volumes of CO(2) and gadodiamide used for diagnostic studies alone versus the volume used for interventional studies was not significantly different (for CO(2), p = 0.09; for gadodiamide, p = 0.30). Eleven major complications occurred in eight patients (5.5%). Two deaths (1.4%) occurred within 30 days. One death was due to cholesterol embolization and the other was not believed to be related to the procedure., Conclusion: Angiography and percutaneous treatment of renal artery stenosis in patients with chronic renal insufficiency and suspected ischemic nephropathy can be performed relatively safely using CO(2) and gadodiamide as angiographic contrast agents without an increased risk of complications. Contrast-induced nephropathy potentially occurred in 3.2% of patients. Neither the degree of underlying renal insufficiency nor diabetes was a risk factor for predicting a greater likelihood of renal function worsening at 48 hr of follow-up. The volumes of CO(2) and gadodiamide used in this study did not result in an increased risk of contrast-involved nephropathy.

In the past two to three decades, the practice among hypertension specialists has been to lower blood pressure with the strong assumption that morbidity and mortality would be reduced. This was largely based on large clinical trials done in the 1960s and 1970s that did not include angiotensin-converting enzyme inhibitors or calcium-channel blockers. Performing large clinical trials is expensive and the results often do not apply to individual patients. Until recently, noninvasive methods to monitor end-organ effects of elevated blood pressure and other cardiovascular risk factors were limited. The development of high-resolution ultrasound and evolving magnetic resonance technology will allow early detection of heart and blood vessel changes and will make monitoring of the progression and regression of disease possible. This will allow better selection of treatment programs for each patient.

Background: Elevated lipoprotein (Lp) (a) concentrations are associated with coronary artery disease and myocardial infarction. Lp(a) is structurally related to proteins involved in lipid transport, fibrinolysis, coagulation, and cellular mitogenesis and is known to have important physiological interactions with the coagulation and fibrinolytic systems. Because these processes may be important to arterial healing after balloon injury, we hypothesized that elevated Lp(a) concentrations may be associated with recurrence of symptoms and restenosis after balloon angioplasty., Methods and Results: We assessed 240 consecutive patients undergoing coronary balloon angioplasty with measurements of Lp(a), total cholesterol, triglycerides, HDL cholesterol, LDL cholesterol, apolipoprotein A-I, and apolipoprotein B-100 concentrations from fresh specimens. Patients were evaluated 4 to 6 months after angioplasty for clinical recurrence by repeat angiography if angina had returned or by maximal exercise treadmill testing with thallium imaging if patients remained asymptomatic. Ninety-seven patients (40%) had clinical recurrence; 143 (60%) did not. Patients with recurrence had significantly greater Lp(a) concentrations compared with those without (median, 29 versus 14; P < .0001). Each patient quintile stratified by increasing Lp(a) concentrations had incrementally greater recurrence rates ranging from 27% (lowest quintile) to 60% (highest quintile). By multivariate logistic regression analysis, Lp(a) concentration was the only predictor of recurrence (P < .0001). A subset of frozen, stored serum samples showed a significant decrease in measured Lp(a) concentration over time (mean, 605 days; P < .01)., Conclusions: An elevated Lp(a) concentration was a risk factor for clinical recurrence after percutaneous transluminal balloon coronary angioplasty. Other lipid levels or clinical characteristics were not significantly associated with recurrence. When serum was frozen and stored for a prolonged period, Lp(a) concentration decreased over time.

A new medical image analysis system to quantify atherosclerosis in the lower abdominal aorta using magnetic resonance imaging is described. This medical image analysis and display system permits the quantification of the three-dimensional (3D) properties of the vessel wall and lumen cross-sectional area and volumes. Preliminary results of employing this medical image analysis capability on magnetic resonance images demonstrated a twofold increase in wall volume per unit vessel length, corresponding to intimal thickening, before luminal narrowing was detected. This work demonstrated the feasibility and usefulness of quantitatively evaluating the 3D properties of the vessel lumen and wall by using a combination of magnetic resonance imaging and image analysis. The demonstration that intimal wall thickening is observed in images before observable occlusion of the lumen can be expected to provide an important early indicator of the future development of atherosclerosis. Such capability will permit detailed and quantitative studies to assess the effectiveness of therapies, such as drug, exercise, and dietary regimens.

Anti-adenosine antibodies were produced in rabbits immunized with N6-carboxymethyladenosine conjugated to methyl albumin. 125I-N6-Aminobenzyladenosine was synthesized and used as a high-specific-activity, high-affinity ligand. A radioimmunoassay (RIA) was developed that can detect 6.25 nM (312.5 fmol) of underivatized adenosine and cross-reacts less than 0.02% with adenine nucleotides and guanosine and not at all with 1 mM inosine. The sensitivity of the RIA can be increased to a detection limit of 0.125 nM (6.25 fmol) by derivitizing samples with benzyl bromide to form N6-benzyladenosine. The assay was adapted to an automated RIA procedure. Assay precision was increased by: (i) inhibiting slight adenosine deaminase activity present in anti-sera; (ii) treating buffers and albumin used in the RIA with charcoal to remove contaminating adenosine; and (iii) correcting for a small but variable component of immunoreactivity not attributable to adenosine. A second antibody prepared with a 2',3'-disuccinyladenosine-albumin conjugate was also found to detect some non-adenosine-mediated immunoreactivity in plasma samples. Immunointerference in human plasma was eliminated in samples treated with ZnSO4/Ba(OH)2 or partially purified over C18 Sep Paks to remove nucleotides and assayed after sample benzylation or succinylation. Human blood was mixed with a novel "stop" solution that was optimized to inhibit adenosine formation from AMP by greater than 99% and to inhibit adenosine uptake into red cells and degradation by greater than 94%. Human plasma/stop solution was assayed by RIA and HPLC with equivalent results.

Attempts to monitor coronary sinus adenosine as a clinical marker of myocardial ischemia in humans have been disappointing. Accordingly, procedures have been developed for detecting adenosine in blood collected from the human coronary sinus. Collection involves using a double-lumen metabolic catheter, which allows blood to be mixed with a stop solution at the catheter tip, thereby minimizing adenosine formation and degradation. A five-component stop solution almost completely arrests adenosine formation and degradation. Adenosine analysis is improved by using both boronate and C18 Sep-Pak columns to purify and concentrate adenosine in human plasma before HPLC. Plasma adenosine in the coronary sinus of patients with and without coronary artery disease, measured before and during peak atrial pacing, showed a twofold atrial pacing-induced increase in adenosine in the patients with coronary artery disease (n = 9, P less than 0.001) but no change in the patients with normal epicardial coronary arteries (n = 6). These preliminary results indicate that coronary sinus adenosine may provide an index of myocardial ischemia in patients with coronary artery disease.

This paper describes an image processing, pattern recognition, and computer graphics system for the noninvasive identification and evaluation of atherosclerosis using multidimensional Magnetic Resonance Imaging (MRI). Particular emphasis has been placed on the problem of developing a pattern recognition system for noninvasively identifying the different plaque classes involved in atherosclerosis using minimal a priori information. This pattern recognition technique involves an extension of the ISODATA clustering algorithm to include an information theoretic criterion (Consistent Akaike Information Criterion) to provide a measure of the fit of the cluster composition at a particular iteration to the actual data. A rapid 3-D display system is also described for the simultaneous display of multiple data classes resulting from the tissue identification process. This work demonstrates the feasibility of developing a "high information content" display which will aid in the diagnosis and analysis of the atherosclerotic disease process. Such capability will permit detailed and quantitative studies to assess the effectiveness of therapies, such as drug, exercise, and dietary regimens.

Radiographic contrast media (RCM) may alter platelet behavior at concentrations achieved during cardiac angiography. We used quenched-flow aggregometry coupled to single-particle counting to study the influence of RCM on the kinetics of platelet aggregation (less than 5.0 sec) induced by adenosine diphosphate (ADP, 2.86 microM). At a concentration in platelet-rich plasma (PRP) of 5 per cent RCM by volume, platelet aggregation was inhibited by diatrizoate, iopamidol and ioxaglate either directly or following incubation of each contrast agent with PRP for 20 minutes. Diatrizoate inhibited more than did iopamidol or ioxaglate (56 +/- 6, versus 39 +/- 3 and 40 +/- 9 per cent respectively; P less than 0.003, p less than 0.009, n = 20 normal subjects). A small reduction (about 16 per cent) in aggregation velocity occurred within 5 seconds of exposure of PRP to all 3 RCM and the onset time (t) or lag period before aggregation begins was significantly prolonged by diatrizoate (p less than 0.03). The RCM vehicles alone (iodinated moiety removed, osmolality readjusted) had no effect on the ADP-induced aggregation. Platelet counts fell significantly after incubation with diatrizoate (12%; p = 0.04). Our data therefore show that early platelet aggregation was inhibited by 3 commonly-used ionic and nonionic contrast agents. Inhibition was apparently caused by the iodinated contrast molecule, began within seconds of platelet-RCM contact and was independent of vehicle composition. Since diatrizoate inhibited aggregation more than iopamidol or ioxaglate, its use may be of additional value during angiographic procedures in clinical situations involving enhanced platelet activation.

The antihypertensive effects of captopril and enalapril maleate were studied over a 10-week period in 24 hypertensive patients randomized into captopril or enalapril treatment groups. Prestudy blood pressure was 171 +/- 4/109 +/- 1 mm Hg and after 4 weeks of hydrochlorothiazide 160 +/- 4/103 +/- 1 (p less than 0.05). With the addition of converting enzyme inhibitor to hydrochlorothiazide the blood pressure decreased at 3 h to 132 +/- 3/87 +/- 2 in the subjects. The diastolic blood pressure decreased acutely more with captopril (-24) than with enalapril (-17) (p less than 0.05). After 10 weeks of combined therapy the depressor response was maintained (134 +/- 3/83 +/- 1) and there was no difference between the diastolic blood pressure in the two groups treated with captopril and enalapril. Acute and chronic responses of plasma renin activity, plasma aldosterone, and converting enzyme to the angiotensin-converting enzyme inhibitor were determined. There was a significant correlation between the acute fall in diastolic blood pressure and rise in plasma renin activity in patients treated with captopril but not with enalapril. In conclusion, there is an acute depressor response with converting enzyme inhibition which is more pronounced with captopril than with enalapril and which correlates with an increase in plasma renin activity. With more prolonged treatment, the two drugs show equivalent efficacy in reducing blood pressure, inhibiting angiotensin-converting enzyme, reducing aldosterone, and stimulating plasma renin activity.

The purpose of this study was to determine whether increased sympathetic nervous system activity with proportionally greater stimulation to the kidney could result in sustained hypertension. This was simulated by continuous intrarenal norepinephrine infusion. Effects of chronic infusion of norepinephrine (0.285 microng/kg per min) into the renal artery and inferior vena cava were compared in uniephrectomized conscious dogs. Ten days of intrarenal norepinephrine infusion produced a sustained rise in mean arterial pressure (25 mm Hg), and a 32-mEg positive sodium balance occurred. Inferior vena caval infusion caused a transient rise, lasting 24 hours, in mean arterial pressure which was associated with a 54-mEq natriuresis. With renal artery infusion, peripheral plasma renin activity rose from 1.0 +/- 00.2 to 4.4 +/- 0.8 ng angiotensin I/ml per hour at 1 hour (P less than 0.002) and fell to 1.4 +/- 0.4 at 24 hours (not significant). Inferior vena caval infusion produced a similar result. [Sar1,ala8]angiotensin II (6 MICrong/kg per min) produced no significant change in arterial blood pressure. (alpha-Adrenergic blockade with phentolamine normalized the blood pressure. Renal plasma flow was chronically decreased by about 25% in dogs given intrarenal norepinephrine; no significant change in glomerular filtration rate occurred. The cardiac output decreased from a control of 7.2 +/- 0.6 to 4.8 +/- 0.1 liters/min (P less than 0.01) and total peripheral resistance was increased from a control of 13 +/- 1 to 26 +/- 1 resistance units (RU) (P less than 0.0005) in dogs given intrarenal norepinephrine. The data indicate that chronic intrarenal infusion of norepinephrine in uninephrectomized conscious dogs results in sustained hypertension characterized by decreased renal plasma flow, normal glomerular filtration rate, positive sodium balance, and increased total peripheral resistance due to norepinephrine-dependent vasoconstriction.

24 hypertensive patients were randomised into 2 groups to compare the antihypertensive effects of enalapril and captopril over a 10-week period. In the hydrochlorothiazide run-in period, blood pressure was reduced from 171 +/- 4/109 +/- 1mm Hg to 160 +/- 4/103 +/- 1mm Hg (p less than 0.05). Angiotensin-converting enzyme (ACE) inhibition decreased blood pressure to 132 +/- 3/87 +/- 2mm Hg. Captopril decreased diastolic blood pressure significantly more after 3 hours than enalapril (-24 versus -17mm Hg, p less than 0.05). After 10 weeks of therapy, this antihypertensive response was maintained at 134 +/- 3/83 +/- 1mm Hg. There was no difference between the captopril and enalapril treated groups. Acute and chronic responses of plasma renin activity, plasma aldosterone and ACE were determined. There was an acute positive correlation between the rise in plasma renin activity and the fall in blood pressures with captopril but not with enalapril. With chronic treatment there was no difference in the ability of either of the 2 drugs to reduce blood pressure, inhibit ACE, reduce aldosterone or stimulate plasma renin activity.

In two patients with end stage renal disease and dialysis-resistant hypertension, the orally active inhibitor of angiotensin-converting enzyme, captopril (SQ14,225; 2-D-methyl-3-mercaptopropranoyl-L-proline, dramatically lowered blood pressure both before and during dialysis. This agent holds promise as an alternate to bilateral nephrectomy in such patients.

Acute bromocriptine administration reduced sitting and standing blood pressure and produced severe orthostatic hypotension in 12 normal subjects. Concomitantly, there was an increase in venous distensibility and basal blood flow, and a decrease in peripheral vascular resistance, as determined by forearm plethysmography. After administration of bromocriptine, plasma norepinephrine concentration decreased. Bromocriptine lowers blood pressure by dilating arterioles and veins, at least in part by means of dopaminergic inhibition of sympathetic nervous system activity.

Coronary artery disease due to atherosclerosis takes the lives of approximately 550,000 Americans each year--an enormous toll. Put in economic terms, the cost to the United States alone has been estimated to exceed 60 billion dollars annually. We have found that well-resolved proton (1H) NMR spectra can be obtained from human atheroma (fatty plaque), despite its macroscopic solid appearance. The fraction of the total spectral intensity corresponding to the sharp 1H NMR signals is temperature dependent and approaches unity at body temperature (37 degrees C). Studies of the total lipids extracted from atheroma and cholesteryl esters were conducted to identify the chemical and physical origin of the spectral signature. The samples were characterized through assignment of their chemical shifts and by measurement of their T1 and T2 relaxation times as a function of magnetic field strength. The results suggest that the relatively sharp 1H NMR signals from human atheroma (excluding water) are due to a mixture of cholesteryl esters, whose liquid-crystalline to isotropic fluid phase transition is near body temperature. Preliminary applications to NMR imaging of human atheroma are reported, which demonstrate early fatty plaque formation within the wall of the aorta. These findings offer a basis for noninvasive imaging by NMR to monitor early and potentially reversible stages of human atherogenesis.