Malignant pericardial effusion.

Malignant pericardial effusion is a common and serious manifestation in malignancies. The origins of the malignant process include solid tumors or hematological malignancies, while primary neoplasms of the pericardium are less common. In the oncological patient, pericardial effusion may develop by several different mechanisms, namely by direct or metastatic spread of the primary process or as a complication of antineoplastic therapies. In some cases, pericardial effusion may be the first manifestation of the disease, and that is why malignancy must be excluded in every case of an acute pericardial disease with cardiac tamponade at presentation, rapidly increasing pericardial effusion and an incessant or recurrent course. Thus, the definite differentiation of malignant pericardial effusion and rapid diagnosis are of particular therapeutic and prognostic importance. Management of these patients is multidisciplinary and requires team work, but at present there is a need for further research. An individual treatment plan should be established, taking into account cancer stage, the patient's prognosis, local availability and experience. In emergency cases with cardiac tamponade or significant effusion, initial relief can be obtained with pericardiocentesis. Despite the magnitude of this serious problem, little progress has been made in the treatment of pericardial effusion secondary to malignant disease.

Diagnostic issues in the clinical management of pericarditis.

AIMS: To review the current major diagnostic issues on the diagnosis of acute and recurrent pericarditis. METHODS: To review the current available evidence, we performed a through search of several evidence-based sources of information, including Cochrane Database of Systematic Reviews, Clinical Evidence, Evidence-based guidelines from National Guidelines Clearinghouse and a comprehensive Medline search with the MeSH terms 'pericarditis', 'etiology' and 'diagnosis'. RESULTS: The diagnosis of pericarditis is based on clinical criteria including symptoms, presence of specific physical findings (rubs), electrocardiographical changes and pericardial effusion. Although the aetiology may be varied, most cases are idiopathic or viral, even after an extensive diagnostic evaluation. In such cases, the course is often benign following anti-inflammatory treatment, and management would be not affected by a more precise diagnostic evaluation. A triage of pericarditis can be safely performed on the basis of the clinical and echocardiographical presentation. Specific diagnostic tests are not warranted if no specific aetiologies are suspected on the basis of the epidemiological background, history and presentation. High-risk features associated with specific aetiologies or complications include: fever > 38 degrees C, subacute onset, large pericardial effusion, cardiac tamponade, lack of response to aspirin or a NSAID. CONCLUSIONS: A targeted diagnostic evaluation is warranted in acute and recurrent pericarditis, with a specific aetiological search to rule out tuberculous, purulent or neoplastic pericarditis, as well as pericarditis related to a systemic disease, in selected patients according to the epidemiological background, presentation and clinical suspicion.

Increased insulin resistance and risk of incident cerebrovascular events in patients with pre-existing atherothrombotic disease.

BACKGROUND AND PURPOSE: Diabetes and the metabolic syndrome are known risk factors for ischaemic stroke. Our aim was to examine whether amongst patients with pre-existing atherothrombotic disease, increased insulin resistance is associated with incident cerebrovascular events. METHODS: Patients with stable coronary heart disease included in a secondary prevention trial were followed up for a mean of 6.2 years. Coronary heart disease was documented by a history of myocardial infarction > or =6 months and <5 years before enrollment and/or stable angina pectoris with evidence of ischaemia confirmed by ancillary diagnostic testing. Main exclusion criteria were insulin treated diabetes, hepatic or renal failure, and disabling stroke. Baseline insulin levels were measured in 2938 patients from stored frozen plasma samples and increased insulin resistance assessed using the homeostatic model assessment of insulin resistance (HOMA-IR), categorized into tertiles or quartiles. RESULTS: Crude rates of incident cerebrovascular events rose from 5.0% for HOMA-IR at the bottom tertile to 5.7% at the middle tertile, and 7.0% at the top tertile (P = 0.07). HOMA-IR at the top versus bottom tertile was associated with an unadjusted hazard ratio (HR) of 1.37 (95%CI, 0.94-1.98) and a 1-unit increase in the ln HOMA-IR was associated with a HR of 1.14 (95%CI, 0.97-1.35). In further analyses adjusting for potential confounders, or categorizing baseline HOMA-IR into quartiles, or excluding diabetic patients, we did not identify an increased risk for incident cerebrovascular events conferred by the top category. CONCLUSIONS: Increased insulin resistance did not predict incident cerebrovascular events amongst patients with pre-existing atherothrombotic disease.

[Recurrent acute idiopathic pericarditis: rheumatologic therapy, autoantibodies and long term outcome]. / Pericardite acuta idiopatica recidivante: terapia reumatologica, autoanticorpi e long term outcome.

OBJECTIVE: To evaluate therapy and rheumatologic aspects of recurrent acute idiopathic pericarditis (RAIP). METHODS: We studied 46 patients. We used non-steroidal anti-inflammatory drugs (NSAIDs) at high dosage. We did not start corticosteroid: if already started, we planned a very slow tapering; 37 patients (80.4%) were treated with colchicine. We also assessed the frequency of ANA, anti-SSA and Rheumatoid factor. RESULTS: With our protocol recurrences dropped from 0.46 to 0.03 attacks/patient/month (p<0.00001) within 12 months and remained at the same level (0.024) till the end of the follow-up (mean 8 years). In the 37 patients treated with colchicine recurrences dropped from 0.5 to 0.03 (p<0.0001) within 12 months, and in 9 patients not given colchicine from 0.27 to 0.045 (p<0.005). When colchicine was used the decrease was significantly higher (0.47 vs 0.23) (p<0.001). In 27 (58.7%) patients ANA were positive at a titre >1/80, in 7 (15.2%) >1/160. Rheumatoid factor was positive in 7 (15.2%) and anti-SSA in 4 (8.7%). During the follow-up 4 (8.7%) new diagnosis of Sjogren and 1 (2.2%) of Rheumatoid Arthritis were made. CONCLUSION: NSAIDs at high dosage, slow tapering of corticosteroid and colchicine are very effective in RAIP. The improvement is more dramatic in colchicine treated patients, but also other patients can achieve good control of the disease. The finding of ANA, anti-SSA and the new rheumatological diagnoses support the involvement of autoimmunity.

Therapy for recurrent acute pericarditis: a rheumatological solution?

OBJECTIVE: To assess the efficacy of a multidrug protocol in recurrent acute pericarditis. We tried also to assess the specific role of colchicine. METHODS: We studied 58 patients (34 males) in the largest monocentric observational study. All patients received prolonged courses of non-steroidal anti-inflammatory drugs; generally we do not start a corticosteroid in recurrent acute pericarditis, but if a steroid had already been started, we planned a very slow tapering; if necessary azathioprine, hydroxychloroquine, and other immunosuppressive drugs were used; 44 patients (27 males, 61.4%) were treated also with colchicine and 14 patients (7 males, 50%) were not given this drug. RESULTS: After starting our protocol recurrences dropped from 0.48 to 0.03 attacks/patient/month (p < 0.00001) within 12 months and remained at the same level till the end of the follow-up (mean 8.1 years) in the whole cohort. In the 44 patients treated with colchicine recurrences dropped from 0.54 to 0.03 attacks/patient/month (p < 0.00001) within 12 months, and in 14 patients not given colchicine recurrences decreased from 0.31 to 0.06 attacks/patient/month (p = 0.002). In patients treated with colchicine the decrease was significantly higher (0.51) than in patients not taking this drug (0.25) (p = 0.006). Colchicine was discontinued by 16.3% of patients because of side effects. CONCLUSION: A multidrug protocol including non-steroidal anti-inflammatory drugs at high dosage, slow tapering of corticosteroid, colchicine, reassurance and close clinical monitoring is very effective in recurrent pericarditis; this improvement is more dramatic in colchicine treated patients, but also patients who do not tolerate it can achieve good control of the disease.

Methylenetetrahydrofolate reductase genotypes and early-onset coronary artery disease.

BACKGROUND: Homozygosity for the common (677C-->T) mutation in the methylenetetrahydrofolate reductase (MTHFR) gene is associated with hyperhomocysteinemia, but there is uncertainty as to the association between this mutation and coronary artery disease (CAD). This study examined the association between MTHFR genotypes and age at onset of CAD. METHODS AND RESULTS: Patients (n=169) with documented myocardial infarction or angiographically documented CAD who were aged < or = 55 years at onset of CAD symptoms and DNA samples from control subjects (n=313) were studied. The prevalence of homozygosity among patients with early CAD onset (aged < or = 45 years) was 28%, which was significantly higher than that in patients with later onset (13%) and in control subjects (14%) (odds ratio 2.4, 95% CI 1.24 to 4.69, P=0.006, and odds ratio 2.7, 95% CI 1.15 to 6.42, P=0.01, respectively). Plasma folate was lower in TT homozygotes who had early CAD onset than in those with later onset (P=0.005). Among patients with plasma folate in the lowest quintile (< or = 12.6 nmol/L), 31% were homozygotes, as were 45% of those with low plasma folate and early CAD onset. There was no difference in the prevalence of traditional risk factors among genotypes. The frequency of homozygosity in patients with < or = 1 risk factor was higher than in those with > or = 2 risk factors (30% versus 12%, P<0.05). In multiple regression analysis, TT homozygosity and plasma folate were independently associated with CAD, but the impact of folate was small. CONCLUSIONS: Homozygosity for the 677C-->T mutation of MTHFR is common and is associated with an increased risk of premature CAD in this population.

The natural history of aortic valve disease after mitral valve surgery.

OBJECTIVES: The present study evaluates the long-term course of aortic valve disease and the need for aortic valve surgery in patients with rheumatic mitral valve disease who underwent mitral valve surgery. BACKGROUND: Little is known about the natural history of aortic valve disease in patients undergoing mitral valve surgery for rheumatic mitral valve disease. In addition there is no firm policy regarding the appropriate treatment of mild aortic valve disease while replacing the mitral valve. METHODS: One-hundred thirty-one patients (44 male, 87 female; mean age 61+/-13 yr, range 35 to 89) were followed after mitral valve surgery for a mean period of 13+/-7 years. All patients had rheumatic heart disease. Aortic valve function was assessed preoperatively by cardiac catheterization and during follow-up by transthoracic echocardiography. RESULTS: At the time of mitral valve surgery, 59 patients (45%) had mild aortic valve disease: 7 (5%) aortic stenosis (AS), 58 (44%) aortic regurgitation (AR). At the end of follow-up, 96 patients (73%) had aortic valve disease: 33 AS (mild or moderate except in two cases) and 90 AR (mild or moderate except in one case). Among patients without aortic valve disease at the time of the mitral valve surgery, only three patients developed significant aortic valve disease after 25 years of follow-up procedures. Disease progression was noted in three of the seven patients with AS (2 to severe) and in six of the fifty eight with AR (1 to severe). Fifty two (90%) with mild AR remained stable after a mean follow-up period of 16 years. In only three patients (2%) the aortic valve disease progressed significantly after 9, 17 and 22 years. In only six patients of the entire cohort (5%), aortic valve replacement was needed after a mean period of 21 years (range 15 to 33). In four of them the primary indication for the second surgery was dysfunction of the prosthetic mitral valve. CONCLUSIONS: Our findings indicate that, among patients with rheumatic heart disease, a considerable number of patients have mild aortic valve disease at the time of mitral valve surgery. Yet most do not progress to severe disease, and aortic valve replacement is rarely needed after a long follow-up period. Thus, prophylactic valve replacement is not indicated in these cases.

Thrombolysis is an effective and safe therapy in stuck bileaflet mitral valves in the absence of high-risk thrombi.

OBJECTIVES: We sought to evaluate the effectiveness and safety of thrombolytic therapy in stuck mitral bileaflet heart valves in the absence of high-risk thrombi. BACKGROUND: Current recommendations for the thrombolytic treatment of stuck prosthetic mitral valves are partially based on older valve models and inclusion of patients in whom high-risk thrombi were either ignored or not sought for. The feasibility and safety of thrombolysis in bileaflet models may be affected by the predilection of thrombi to catch the leaflet hinge. METHODS: We studied 12 consecutive patients (men/women = 5/7, age 58.8 +/- 14.9 years) who experienced one or more episodes of stuck bileaflet mitral valve over a 33-month period and received thrombolytic therapy with streptokinase, urokinase or tissue-type plasminogen activator. Transesophageal echocardiography was performed in all patients. Patients with mobile or large (>5 mm) thrombi were excluded. Functional class at initial episode was I-II in 4 patients (33.3%) and III-IV in 8 patients (66.6%). RESULTS: Patients receiving thrombolytic therapy achieved an overall 83.3% freedom from a repeat operation or major complications (95% confidence interval 51.6-97.9%). Minor bleeding occurred in three patients (25%) and allergic reaction in one (8.3%). Transient vague neurologic complaints, without subjective findings, occurred in four patients (33.3%). Three patients had one or more relapses within 5.2 +/- 3.1 months from the previous episode, and readministration of thrombolytics was successful. CONCLUSIONS: In clinically stable patients with stuck bileaflet mitral valves and no high-risk thrombi, thrombolysis is highly successful and safe, both in the primary episode and in recurrence. The best thrombolytic regimen is yet to be established.

Persistent ST segment depression in precordial leads V5-V6 after Q-wave anterior wall myocardial infarction is associated with restrictive physiology of the left ventricle.

OBJECTIVES: To examine the relationship between the persistence of ST segment depression in leads V5-V6 after Q-wave anterior wall myocardial infarction (MI) and the filling pattern of the left ventricle (LV). BACKGROUND: Precordial ST segment depression predominantly in leads V5-V6 is associated with increased in-hospital morbidity and mortality after acute myocardial ischemia, perhaps due to reduced diastolic distensibility of the LV. METHODS: We prospectively studied 19 patients after Q-wave anterior wall MI (>6 months). All patients underwent 12-lead ECG recording, symptom-limited treadmill exercise testing with single photon emission computed tomography thallium-201 imaging, transthoracic Doppler echocardiography, cardiac catheterization and measurement of circulating atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) levels. Patients were classified based on the presence of ST segment depression in leads V5-V6: Group I = ST segment depression <0.1 mV (n = 10); Group II = ST segment depression > or =0.1 mV (n = 9). RESULTS: Patients in Group II had greater LV end diastolic pressures (32.4 +/- 6.5 mm Hg vs. 14.8 +/- 6.1 mm Hg; p = 0.0001), higher plasma ANP (44.4 +/- 47.1 pg/ml vs. 10.7 +/- 14 pg/ml; p = 0.04) and BNP levels (89.4 +/- 62.7 pg/ml vs. 23.6 +/- 33.1 pg/ml; p = 0.01), greater left atrium area (20.6 +/- 3.1 cm2 vs. 17.8 +/- 2.4 cm2; p = 0.05), lower peak atrial (A), higher early (E) mitral inflow velocities, a higher E/A ratio and a lower deceleration time (167 +/- 44 ms vs. 220 +/- 40 ms; p = 0.05). Lung thallium uptake during exercise was more common in Group II (78% vs. 10%, p = 0.04). CONCLUSIONS: Persistent ST segment depression in leads V5-V6 in survivors of Q-wave anterior wall MI is associated with increased LV filling pressure and a restrictive LV filling pattern.

Mitral annulus calcification--a window to diffuse atherosclerosis of the vascular system.

Mitral annulus calcification (MAC) is a chronic, non-inflammatory, degenerative process of the fibrous support structure of the mitral valve. It occurs more often in women and the elderly. MAC is associated with known atherosclerotic risk factors such as diabetes mellitus, hypertension and hypercholesterolemia. It is also known that patient with MAC have higher prevalence of left atrial and left ventricular enlargement, hypertrophic cardiomyopathy, atrial fibrillation, aortic valve calcification and stenosis, various cardiac conduction defects, bacterial endocarditis, cardiovascular events and stroke, though the etiological basis is unknown. Pathological studies from the 80s present a theory that MAC is a form of atherosclerosis. In order to test this theory we conducted during the last years a few clinical studies to examine the association of MAC and known atherosclerotic phenomena. We found higher prevalence of aortic atheroma in patients with MAC and atheroma thickness. We also found in MAC patients higher prevalence of carotid artery stenosis, coronary artery stenosis, peripheral artery stenosis and higher levels of beta2-Glycoprotein I antibodies in patients with MAC thickness equal or greater than 5 mm. These studies support the theory that MAC is a form of atherosclerosis and define a group of patients with higher prevalence of atherosclerotic disease in multiple blood vessels. The purpose of this review is to summarize the data concerning MAC and atherosclerotic processes, emphasizing that MAC in itself may be an atherosclerotic process.

Association between mitral annulus calcification and aortic atheroma: a prospective transesophageal echocardiographic study.

BACKGROUND AND PURPOSE: Although mitral annulus calcification (MAC) has been reported to be a significant independent predictor of stroke, no causative relationship was proven. It is also known that aortic atheroma (AA), especially those >/=5 mm thick and/or protruding and/or mobile are associated with stroke. This study was designed to determine whether an association exists between MAC and AA. METHODS: We prospectively evaluated the records of 279 consecutive patients who underwent transesophageal echocardiography (TEE) for various indications to measure the presence and characteristics of AA. The 105 patients in whom a diagnosis of MAC was made on transthoracic echocardiography (TTE) immediately preceding the TEE, were compared with 174 age-matched patients without MAC. MAC was defined as a dense, localized, highly reflective area at the base of the posterior mitral leaflet. We measured MAC thickness with two-dimensional-TTE in four-chamber view and AA thickness, protrusion and mobility with TEE. AA was defined as localized intimal thickening of >/=3 mm. A lesion was considered complex if there was plaque extending >/=5 mm into the aortic lumen and/or if it was protruding, mobile or ulcerated. RESULTS: No differences were found between the groups in risk factors for atherosclerosis or in indications for referral for TEE. Significantly higher rates were found in the MAC group for prevalence of AA (91 vs. 44%, P<0.001), atheromas >/=5 mm thick (68 vs. 19%, P<0.001), protruding atheromas (44 vs. 15%, P<0.001), ulcerated atheromas (10 vs. 1%, P<0.001) and complex atheroma (74 vs. 22%, P<0.001). Sixty patients had MAC thickness >/=6 mm and 45<6 mm. AA thickness was significantly greater in the patients with a MAC thickness of >/=6 mm (6.1+/-2.8 vs. 5.0+/-2.6 mm, P=0.03). On multivariate analysis MAC, hypertension and age were the only independent predictors of AA (P=0.0001, 0.005 and 0.007, respectively). CONCLUSIONS: There is a significant association between the presence and severity of MAC and AA. MAC may be an important marker for atherosclerosis of the aorta. This association may explain in part the high prevalence of systemic emboli and stroke in patients with MAC.

Anti-oxidized low density lipoprotein antibody determination as a predictor of restenosis following percutaneous transluminal coronary angioplasty.

Recent data suggests that autoimmune factors play an important role in the pathogenesis of atherosclerosis. In this context several autoantigens have been shown to elicit an immune response that results in accelerated atherosclerotic plaque formation. In the present study, we investigated whether elevated titers of anti-oxidized low density lipoprotein (oxLDL), anticardiolipin and antibodies to beta2-glycoprotein I (beta2GPI) can predict subsequent restenosis in patients undergoing percutaneous transluminal coronary angioplasty (PTCA). A total of 74 consecutive patients (52 males, 22 females) with coronary artery disease were enrolled in the study. All patients underwent successful PTCA prior to which blood was drawn for the antibody analysis. The PTCA was followed by a clinical evaluation. Patients with recurrent chest pains underwent a repeated angiography and 34 of the 74 patients (46%) experienced restenosis. Patients positive for the presence of anti-oxLDL antibodies were more likely to develop restenosis within 6 months when compared with patients with no subsequent restenosis (relative-risk of 1.87; P< 0.05). Presence of anti-oxLDL antibodies was associated with hyperlipidemia (r = 0.25; P < 0.05) but not with other risk factors for atherosclerosis. Positivity for anticardiolipin or anti-beta2GPI antibodies which associate with a prothrombotic state, was not effective in predicting lumen narrowing. Thus, the presence of elevated levels of anti-oxLDL antibodies is associated with a higher risk for coronary restenosis following PTCA.

New electrocardiographic criteria for predicting either the right or left circumflex artery as the culprit coronary artery in inferior wall acute myocardial infarction.

Two readily obtainable measurements on the admission electrocardiogram-a higher ST-segment elevation in lead III than in lead II and a greater ST-segment depression in lead aVL than in lead I-can distinguish right coronary artery from left circumflex artery-related acute inferior wall myocardial infarction.

Comparison of patients with inferior wall acute myocardial infarction with versus without ST-segment elevation in leads V5 and V6.

One hundred forty-one patients with first acute inferior wall myocardial infarction were examined. ST-segment elevation in precordial leads V5 to V6 was found in 34; 94% of them had "mega-artery" compared with 2% in those without ST-segment elevation in precordial leads V5 to V6.

Electrocardiographic criteria for predicting the culprit artery in inferior wall acute myocardial infarction.

Two patterns of the QRS complex in the lateral lead aVL on the admission electrocardiograms of patients with inferior wall acute myocardial infarction (AMI) were correlated with the culprit artery. S/R wave ratio < or =1/3 with ST depression < or =1 mm was found to be a sensitive and specific marker for left circumflex artery AMI, whereas S/R-wave ratio >1/3 with ST-segment depression >1 mm was suggestive of right coronary artery AMI.

Effectiveness of coronary stent deployment without predilation.

The feasibility of coronary stenting without predilation is demonstrated in 240 patients. In all, 249 stents were placed. Primary implantation was successful in 93% of cases. In 17 lesions the stents could not be advanced through the stenotic lesion. The unexpanded stents were removed through the guiding catheter, and stenting was performed after prediction. Minor complications (side branch compromise and intimal dissection), which were successfully treated, occurred in 26 patients (10.6%).

Nonobstructive aortic valve calcium as a window to atherosclerosis of the aorta.

Aortic valve calcium without stenosis and mitral annulus calcium (MAC) are known to correlate with atherosclerotic risk factors. Recently, it has been reported that MAC is associated with atherosclerosis of the cardiovascular system, suggesting MAC as an atherosclerotic process by itself. Hence, the aim of the present study was to determine whether a similar association between aortic valve calcium and aortic atheroma exists. Ninety-six patients (54 men and 42 women, mean age 72 +/- 12 years) with aortic valve calcium who underwent transesophageal echocardiography (TEE) formed the study group. They were compared with 92 sex- and age-matched patients without aortic valve calcium who underwent TEE for the same indications during the same period. The presence and echocardiographic features of aortic atheromas were evaluated by TEE. No differences were found between the groups in risk factors for atherosclerosis or in indications for referral for TEE. Significantly higher rates were found in the aortic valve calcium group for prevalence of aortic atheroma (86% vs 30%, p = 0.001). This significant trend was also consistent with the dimension and complexity of the atheromas. On multivariate analysis aortic valve calcium, and MAC were the only independent predictors of aortic atheroma (p = 0.0001, 0.006 respectively). We conclude that there is a significant association between the presence of aortic valve calcium and the presence and severity of aortic atheroma. Thus, aortic valve calcium may serve as a window to atherosclerosis of the aorta.

Mitral annular calcium detected by transthoracic echocardiography is a marker for high prevalence and severity of coronary artery disease in patients undergoing coronary angiography.

This study tests the hypothesis that mitral annular calcium (MAC) detected by transthoracic echocardiography (TTE) is a marker for high prevalence and severity of coronary artery disease (CAD) in patients undergoing coronary angiography. Pathological studies have suggested that there is an association between MAC and calcific deposits in coronary arteries; however, there are no clinical data to support this association. One hundred sixty-five patients with MAC (101 women and 64 men; mean age 71 +/- 8 years) who underwent cardiac catheterization with coronary angiography for various reasons were compared with 147 age-matched controls without MAC who underwent coronary angiography for the same indications during the same period. MAC was defined as a dense, localized, highly reflective area at the base of the posterior mitral leaflet detected by TTE. Obstructive CAD was defined as either > or = 50% reduction of the internal diameter of the left main coronary artery or > or = 70% reduction of the internal diameter of the left anterior descending, right coronary, or left circumflex artery distribution. Compared with controls, the MAC group had a significantly higher prevalence of CAD (89% vs 75%, p = 0.001) and higher rates of 3-vessel disease (45% vs 24%, p = 0.001) and left main CAD (13% vs 5%, p = 0.009). Nonsignificant CAD was more common in the control group (25% vs 11%, p = 0.001). Multivariate analysis identified MAC (p = 0.0002), indications for cardiac angiography (p = 0.02), sex (p = 0.03), and diabetes mellitus (p = 0.03) as independent predictors for the presence and severity of obstructive CAD. MAC detected by TTE may be a marker for high prevalence and severity of CAD in patients undergoing coronary angiography.

Association between mitral annular calcium and aortic atheroma as detected by transesophageal echocardiographic study.

Significant association was found between the presence of mitral annular calcium (MAC) and aortic atheroma detected by transesophageal echocardiography. MAC may be an important marker for aortic atherosclerosis.

Relation of nonobstructive aortic valve calcium to carotid arterial atherosclerosis.

Recently it was shown that subjects with aortic valve calcium (AVC) are at increased risk for future cardiovascular disease including stroke. We hypothesized that the increased risk of stroke may be due to an association with carotid artery atherosclerotic disease. Between 1995 and 1999 our laboratory made a diagnosis of AVC without significant stenosis in 3,949 patients. Of those, 279 patients without other cardiac structural exclusion criteria (148 men and 131 women; mean age 73 +/- 9 years, range 45 to 90) underwent carotid artery duplex ultrasound for various indications, and formed the study group. Age- and sex-matched patients without AVC (n = 277), who underwent carotid artery duplex ultrasound during the same period and for the same indications, served as the control group. Compared with the control group, the AVC group had a significantly higher prevalence of carotid stenosis (> 40% to 60%, 89% vs 78% [p < 0.001]; >60% to 80%, 43% vs 23% [p <0.001];and > 80% to 100%, 32%vs 14% [p < 0.001]). The AVC group had a similar, significantly higher prevalence of > or = 2-vessel disease and bilateral carotid stenosis (stenosis levels of > 20% to 40%, >40% to 60%, > 60% to 80%, and > 80% to 100%). In multivariate analysis, AVC, but not traditional risk factors, was the only independent predictor of severe carotid atherosclerotic disease (stenosis > 80% to 100%; p = 0.0001). Thus, there is a significant association between the presence of AVC and carotid atherosclerotic disease.