Biomedical subjects
Publications and source records attributed to Y Agmon.
A case report of a patient with acute myocardial infarction and severe hypoxemia due to acute right to left interatrial shunt (RLIAS) is presented. Diagnostic and therapeutic procedures are discussed.
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OBJECTIVES: The aim of this study was to examine the association between atherosclerosis risk factors, aortic atherosclerosis and aortic valve abnormalities in the general population. BACKGROUND: Clinical and experimental studies suggest that aortic valve sclerosis (AVS) is a manifestation of the atherosclerotic process. METHODS: Three hundred eighty-one subjects, a sample of the Olmsted County (Minnesota) population, were examined by transthoracic and transesophageal echocardiography. The presence of AVS (thickened valve leaflets), elevated transaortic flow velocities and aortic regurgitation (AR) was determined. The associations between atherosclerosis risk factors, aortic atherosclerosis (imaged by transesophageal echocardiography) and aortic valve abnormalities were examined. RESULTS: Age, male gender, body mass index (odds ratio [OR]: 1.07 per kg/m(2); 95% confidence interval [CI]: 1.02 to 1.12), antihypertensive treatment (OR: 1.93; CI: 1.12 to 3.32) and plasma homocysteine levels (OR: 1.89 per twofold increase; CI: 0.99 to 3.61) were independently associated with an increased risk of AVS. Age, body mass index and pulse pressure (OR: 1.21 per 10 mm Hg; CI: 1.00 to 1.46) were associated with elevated (upper quintile) transaortic velocities, whereas only age was independently associated with AR. Sinotubular junction sclerosis (p = 0.001) and atherosclerosis of the ascending aorta (p = 0.03) were independently associated with AVS and elevated transaortic velocities, respectively. CONCLUSIONS: Atherosclerosis risk factors and proximal aortic atherosclerosis are independently associated with aortic valve abnormalities in the general population. These observations suggest that AVS is an atherosclerosis-like process involving the aortic valve.
OBJECTIVE: To examine the association between atrial fibrillation (AF) and aortic atherosclerosis in the general population. SUBJECTS AND METHODS: Transesophageal echocardiography was performed in 581 subjects, a random sample of the adult Olmsted County, Minnesota, population (45 years of age or older) participating in the Stroke Prevention: Assessment of Risk in a Community (SPARC) study. The frequency of aortic atherosclerosis was determined in 42 subjects with AF and compared with that in 539 subjects without AF (non-AF group). RESULTS: Subjects with AF were significantly older than non-AF subjects (mean +/- SD age, 82+/-10 vs 66+/-13 years, respectively; P<.001) and more commonly had hypertension (28 [66.7%] vs 288 [53.4%], respectively; P=.10). The 2 groups were similar in sex and frequency of diabetes mellitus, hyperlipidemia, or smoking history (P>.10). The odds of aortic atherosclerosis (of any degree) were 2.87 times greater (95% confidence interval [CI], 1.41-5.83; P=.004) and the odds of complex atherosclerosis (protruding atheroma >4 mm thick, mobile debris, or plaque ulceration) were 2.71 times greater (CI, 1.13-6.53; P=.03) in the AF group than in the non-AF group. Age was a significant predictor of aortic atherosclerosis (P<.001). After adjusting for age, the odds of atherosclerosis and complex atherosclerosis were not significantly different between the 2 groups (P=.13 and P=.75, respectively). CONCLUSIONS: In the general population, AF is associated with aortic atherosclerosis, including complex atherosclerosis. This association is related to age since both AF and aortic atherosclerosis are more frequent in the elderly population.
BACKGROUND: Atherosclerosis of the thoracic aorta is associated with stroke. The association between hypertension, a major risk factor for stroke, and aortic atherosclerosis has not been determined in the general population. METHODS AND RESULTS: Transesophageal echocardiography was performed in 581 subjects, a random sample of the Olmsted County (Minnesota) population aged >/=45 years participating in the Stroke Prevention: Assessment of Risk in a Community (SPARC) study. Blood pressure was assessed by multiple office measurements and 24-hour ambulatory blood pressure monitoring. The association between blood pressure variables and aortic atherosclerosis was evaluated by multiple logistic regression, adjusting for other associated variables. Among subjects with atherosclerosis, blood pressure variables associated with complex aortic atherosclerosis (protruding plaques >/=4 mm thick, mobile debris, or ulceration) were determined. Age and smoking history were independently associated with aortic atherosclerosis of any degree (P:</=0.001) and with complex atherosclerosis (P:=0.002), whereas sex, diabetes mellitus, and body mass index were not. Multiple systolic and pulse pressure variables (office and ambulatory), but none of the diastolic blood pressure variables, were associated with atherosclerosis and complex atherosclerosis, adjusting for age and smoking. Among subjects with atherosclerosis, the odds of complex atherosclerosis increased as ambulatory out-of-bed systolic blood pressure increased (odds ratio 1.43 per 10 mm Hg increase, 95% CI 1. 10 to 1.87) and with hypertension treatment, adjusting for age and smoking history. CONCLUSIONS: High blood pressure is independently associated with aortic atherosclerosis. Among subjects with atherosclerosis, high blood pressure is associated with complex atherosclerosis.
The objectives of this study were to establish reference values and define the determinants of left atrial appendage (LAA) flow velocities in the general population. LAA flow velocities (contraction and filling velocities) were assessed by transesophageal echocardiography in 310 subjects aged > or = 45 years, sampled from the population-based Stroke Prevention: Assessment of Risk in a Community study. All subjects were in sinus rhythm, with preserved left ventricular systolic function (ejection fraction > or = 50%), and without valvular disease. Values of LAA contraction and filling velocities were established for various age groups in the population. Age was negatively associated with LAA contraction and filling velocities, which decreased by 4.1 cm/s (p < 0.001) and 2.0 cm/s (p < 0.01) for every 10 years of age, respectively. Contraction velocities were 5 cm/s higher in men than in women (p < 0.05). After adjusting for age and sex, heart rate was independently associated with LAA contraction velocities (p < 0.001; nonlinear association). Body surface area, left atrial size, left ventricular mass index, and a history of previous cardiac disease or hypertension showed no significant association with LAA flow velocities (p > 0.05). Furthermore, detailed analysis of 24-hour ambulatory blood pressure data (available in 253 subjects) showed no association between various blood pressure parameters (systolic and diastolic blood pressure, out-of-bed and in-bed measurements) and LAA flow velocities (all p > 0.05). In summary, the present study establishes the reference values for LAA flow velocities in a large sample of the general population. LAA flow velocities progressively decline with age in subjects with preserved left ventricular systolic function.
The effect of volume reduction on various diastolic Doppler parameters of left ventricular filling was assessed in 13 patients before and after hemodialysis. Volume reduction decreased early diastolic mitral annular velocities to a lesser extent than early diastolic mitral inflow velocities.
BACKGROUND: Atrial septal aneurysm (ASA) is a putative risk factor for cardioembolism. However, the frequency of ASA in the general population has not been adequately determined. Therefore, the frequency in patients with cerebral ischemic events, compared with the frequency in the general population, is poorly defined. We sought to determine the frequency of ASA in the general population and to compare the frequency of ASA in patients with cerebral ischemic events with the frequency in the general population. METHODS AND RESULTS: The frequency of ASA in the population was determined in 363 subjects, a sample of the participants in the Stroke Prevention: Assessment of Risk in a Community study (control subjects), and was compared with the frequency in 355 age- and sex-matched patients undergoing transesophageal echocardiography in search of a cardiac source of embolism after a focal cerebral ischemic event. The proportion with ASA was 7.9% in patients versus 2.2% in control subjects (P=0.002; odds ratio of ASA, 3.65; 95% CI, 1.64 to 8.13, in patients versus control subjects). Patent foramen ovale (PFO) was detected with contrast injections in 56% of subjects with ASA. The presence of ASA predicted the presence of PFO (odds ratio of PFO, 4.57; 95% CI, 2.18 to 9.57, in subjects with versus those without ASA). In 86% of subjects with ASA and cerebral ischemia, transesophageal echocardiography did not detect an alternative source of cardioembolism other than an associated PFO. CONCLUSIONS: The prevalence of ASA based on this population-based study is 2.2%. The frequency of ASA is relatively higher in patients evaluated with transesophageal echocardiography after a cerebral ischemic event. ASA is frequently associated with PFO, suggesting paradoxical embolism as a mechanism of cardioembolism. In patients with cerebral ischemia and ASA, ASA (with or without PFO) commonly is the only potential cardioembolic source detected with transesophageal echocardiography.
The left atrial (LA) appendage is a common source of cardiac thrombus formation associated with systemic embolism. Transesophageal echocardiography allows a detailed evaluation of the structure and function of the appendage by two-dimensional imaging and Doppler interrogation of appendage flow. Specific flow patterns, reflecting appendage function, have been characterized for normal sinus rhythm and various abnormal cardiac rhythms. Appendage dysfunction has been associated with LA appendage spontaneous echocardiographic contrast, thrombus formation and thromboembolism. These associations have been studied extensively in patients with atrial fibrillation or atrial flutter, in patients undergoing cardioversion of atrial arrhythmias and in patients with mitral valve disease. The present review summarizes the literature on the echocardiographic assessment of LA appendage structure, function and dysfunction, which has become an integral part of the routine clinical transesophageal echocardiographic examination.
Noncompaction of the ventricular myocardium is a rare congenital cardiomyopathy resulting from an arrest in normal endomyocardial embryogenesis. The characteristic echocardiographic findings consist of multiple, prominent myocardial trabeculations and deep intertrabecular recesses communicating with the left ventricular cavity. The disease uniformly affects the left ventricle, with or without concomitant right ventricular involvement, and results in systolic and diastolic ventricular dysfunction and clinical heart failure. Noncompaction was initially described in children. However, recent studies have characterized this disease in the adult population, in whom this process may be more prevalent than currently appreciated. We describe an illustrative case of isolated noncompaction of the ventricular myocardium in a 57-year-old woman with the typical clinical and echocardiographic features of the disease. The literature on the topic is reviewed.
The response of insulin-like growth factor (IGF) I in acute renal failure was evaluated in a model of radiocontrast nephropathy associated with selective necrosis of medullary thick ascending limbs. In brief, rats were administered radiocontrast medium or vehicle injections for controls after combined inhibition of prostanoids and nitric oxide. Twenty-four hours after the insult, tissue mRNAs for IGF-I, the IGF-I receptor, and IGF-binding proteins (IGFBP) 1 and 3 were assayed in cortex, medulla, and liver by solution hybridization-RNase protection assay, and IGFBPs were measured in serum and tissue by Western ligand blotting. Cortical IGF-1 increased, whereas medullary IGF-I mRNA decreased. Renal IGFBPs decreased, whereas IGFBP-1 mRNA increased. The IGF system in the liver was unchanged. We conclude that general changes in renal IGFBPs in this experimental model of acute renal failure might increase the level of cortical IGF-I in a way that could modulate medullary recovery.
OBJECTIVE: This study was designed to detect changes in complement levels following acute myocardial infarction and to test whether magnesium sulphate (MgSO4) administration interferes with the complement response that follows acute myocardial infarction. DESIGN: Twenty-nine patients with acute myocardial infarction treated with streptokinase were included and randomly assigned to three treatment groups. In groups A and B, a bolus of 1 g MgSO4 was infused intravenously followed by 4 g (group A) and 14 g (group B) MgSO4 for 24 h while normal saline was administered in group C (control). Blood samples for C3, C4 and CH-100 were obtained at baseline and repeatedly during the 48 h following the initiation of magnesium infusion. RESULTS: In groups A and C, a remarkable decrease in the levels of C3, C4 and CH-100 was observed when measured 1 h after the end of streptokinase infusion and thereafter for the ensuing 48 h compared to baseline values (P < 0.05). In group B, the decrease in these complement elements was attenuated, and a significant (P < 0.05) delayed decrease of C3 and C4 was observed only at 24 h and later up to 48 h. The mean level of CH-100 in group B was significantly depressed compared to baseline from 3 h and thereafter up to 48 h. Mean C3 values plotted against observation time differed between the three groups (P = 0.021). A similar trend was observed for C4 (P = 0.133) but not for CH-100 (P = 0.46). CONCLUSION: (1) Complement elements are being consumed following acute myocardial infarction treated by streptokinase. (2) High-dose intravenous magnesium attenuates the complement process following acute myocardial infarction. (3) These results might signify that magnesium modulates the inflammatory response that follows infarction.
To study renal cortical and medullary oxygen tensions, we used sensitive Clark-type O2 microelectrodes, inserted by micromanipulators into the cortex and medulla of kidneys of anesthetized rats. As previously reported, under basal conditions, medullary PO2 was significantly lower than cortical PO2. Furosemide, which inhibits reabsorptive transport in the medullary thick ascending limb, increased medullary PO2 from 16 +/- 4 to 35 +/- 4 mmHg (P < 0.0005) without altering cortical PO2. This effect, reproduced by ethacrynic acid and bumetanide, was selective for loop diuretics and was directly due to decreased tubular O2 consumption, since medullary blood flow was remarkably reduced by furosemide (-28 +/- 6% from baseline, P < 0.0001, as measured by a laser-Doppler probe). By contrast, acetazolamide, which decreases proximal tubule metabolism, selectively increased cortical PO2. These data are, in general, consistent with tubular metabolism as a major determinant of intrarenal oxygenation and suggest, in particular, that medullary reabsorptive work is at least in part responsible for renal medullary hypoxia.
Human radiocontrast nephrotoxicity is predicted by the presence of multiple risk factors, often associated with compromised renal circulation. To produce a simple model of radiocontrast nephropathy, rats were pretreated with indomethacin and N omega-nitro-L-arginine methyl ester (L-NAME, to inhibit nitric oxide synthesis) before the administration of iothalamate. Acute renal failure consistently developed, with a decline in creatinine clearance from 1.05 +/- 0.10 to 0.27 +/- 0.05 ml/min (P < 0.001) associated with selective necrosis of 49 +/- 9% of medullary thick ascending limbs. Hemodynamic studies using laser-Doppler probes revealed that when injected alone, iothalamate increased outer medullary blood flow to 196 +/- 25% of baseline (P < 0.001). Pretreatment by L-NAME or indomethacin both reduced basal medullary blood flow and transformed the medullary vasodilator response to radiocontrast into vasoconstriction, with a prolonged reduction of medullary blood flow to less then half of baseline. Combined administration of indomethacin, L-NAME, and iothalamate lowered medullary blood flow to 12 +/- 4% of baseline. We conclude that prostanoids and nitric oxide have an important protective role in the renal response to radiocontrast material. Reduced synthesis of these vasoactive substances in renal/vascular diseases may predispose patients to radiocontrast nephropathy.
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