Left ventricular pseudoaneurysm associated with systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is associated with several cardiac manifestations but, to our knowledge, there have been no previously published reports on left ventricular (LV) pseudoaneurysm in this disease. We describe a case of a 30-year-old woman with SLE who presented with a disease flare (acute and subacute cutaneous lupus, pericarditis, fever, leukopenia) associated with heart failure syndrome. The patient was diagnosed with a large LV pseudoaneurysm and a bovine pericardium patch closure was performed. Coronary arteries were angiographically normal, and cardiac magnetic resonance imaging did not exhibit detectable myocardial fibrosis or infarction. Trauma, previous cardiac surgery, Chagas disease, and antiphospholipid syndrome were excluded. Histopathology of the pericardium revealed lymphocytic arteriolitis raising the possibility of an autoimmune-mediated mechanism for this complication. The unequivocal concomitant diagnosis of lupus flare, the exclusion of other causes of pseudoaneurysm and the histopathological finding of arteriolitis in this patient reinforces the hypothesis of lupus-mediated lesion.

Chronic thromboembolic and pulmonary arterial hypertension share right ventricular and pulmonary artery CMR features.

BACKGROUND: Cardiac magnetic resonance (CMR) imaging has gained importance in pulmonary hypertension (PH) and studies have demonstrated its use as a surrogate marker and in following treatment of these patients. The pathophysiology of PH differs between pulmonary arterial hypertension (PAH, group 1) and chronic thromboembolic PH (CTEPH, group 4). OBJECTIVES: The present study tested the hypothesis that PAH and CTEPH display different characteristics on CMR imaging. METHODS: 46 patients were evaluated for pulmonary vascular disease in the French National Reference Center for PH (23 PAH and 23 CTEPH matched for age and gender). All patients had the right heart catheterization (RHC) and CMR imaging performed within 48h. CMR imaging was performed on a 1.5 T scanner. RESULTS: PAH and CTEPH had similar body surface area and similar invasive hemodynamics, including mean pulmonary arterial pressure, cardiac index, pulmonary vascular resistance and right atrial pressure. PAH and CTEPH had similar CMR data. Right ventricular (RV) morphology and function and pulmonary artery (PA) data were also similar. CONCLUSION: Age- and sex-matched PAH and CTEPH patients displayed similar values of the CMR indices of RV and PA morphology and function, suggesting that the RV-PA responses are similar in both groups, mostly related to the overall increase in after load.

Red wine consumption, coronary calcification, and long-term clinical evolution.

Coronary artery calcification (CAC) is associated with atherosclerotic complications. However, elevated CAC may not always imply a worse prognosis. Herein, we report the clinical evolution of long-term red wine (RW) drinkers in relation to CAC. We followed 200 healthy male habitual RW drinkers and compared them to 154 abstainers for a period of 5.5 years. The initial evaluation included coronary computed tomography angiography (CTA), clinical, demographics, and laboratory data. CAC was quantified by the Agatston score. The follow-up process was conducted by telephone calls and/or hospital record review. The composite end-point of total death, acute myocardial infarction (AMI), or coronary revascularization (or major adverse cardiac event - MACE) was assessed. The RW drinkers ingested 28.9±15 g of alcohol/day for 23.4±12.3 years. They had higher high-density lipoprotein and low-density lipoprotein, but lower C-reactive protein than abstainers. Age, total cholesterol, triglycerides, glucose, and liver enzymes were similar. History of diabetes was lower among drinkers, but other risk factors were similar. However, drinkers had higher CAC than abstainers; the mean value was 131.5±362 in drinkers vs 40.5±320 in abstainers (P<0.001). The median and interquartile range were 15 (0.0-131.5) in RW drinkers and 1 (0.0-40.5) in abstainers (P=0.003). During the follow-up, MACE was significantly lower in drinkers than in abstainers, despite their higher CAC. The difference was driven mainly by AMI (0 vs 6; P<0.03). Greater CAC values in this setting did not predict worse prognosis. A possible underlying mechanism is lesion calcification, which leads to plaque stabilization and less clinical events.

Microvascular integrity and the time course of myocardial sodium accumulation after acute infarction.

Loss of membrane permeability caused by ischemia leads to cellular sodium accumulation and myocardial edema. This phenomenon has important implications to left ventricular structure and function in the first hours after myocardial infarction. We hypothesized that during this period of time, after prolonged coronary occlusion and complete reflow, the rate of myocardial sodium accumulation is governed by microvascular integrity. We used 3-dimensional (23)Na MRI to monitor myocardial sodium content changes over time in an in vivo closed-chest canine model (n=13) of myocardial infarction and reperfusion. Infarcts with microvascular obstruction (MO) defined by both radioactive microspheres and contrast-enhanced (1)H MRI showed a slower rate of sodium accumulation as well as lower blood flow at 20 minutes and 6 hours after reperfusion. Conversely, the absence of MO was associated with faster rates of sodium accumulation and greater blood flow restoration. In addition, infarct size by (23)Na MRI correlated best with infarct size by triphenyltetrazolium chloride and contrast-enhanced (1)H MRI at 9 hours after reperfusion. We conclude that in reperfused myocardial infarction, sodium accumulation is dependent on microvascular integrity and is slower in regions of MO compared with those with patent microvasculature. Finally, (23)Na MRI can be a useful tool for monitoring in vivo myocardial sodium content in acute myocardial infarction.

Relationship between glycemic control and coronary artery disease severity, prevalence and plaque characteristics by computed tomography coronary angiography in asymptomatic type 2 diabetic patients.

Evaluate whether glycemic control in type 2 diabetes (DM2) asymptomatic for coronary artery disease (CAD) affects not only the presence and magnitude of CAD but also the characteristics of plaque vulnerability using multidetector row computed coronary tomography (MDCT). Acute coronary syndrome (ACS) is frequently observed in asymptomatic DM2 patients. Positive vessel remodeling (PR) and low-attenuation plaques (LAP) identified by MDCT have been demonstrated to be characteristics of subsequent culprit lesions of ACS. However, little is known regarding plaque characteristics in asymptomatic diabetic patients and their relationship with glycemic control. Ninety asymptomatic DM2 patients, aged 40-65 years old, underwent MDCT. The presence of atherosclerotic obstruction, defined as coronary stenosis ≥50 %, and plaque characteristics were compared between two groups of patients with A1c < 7 and A1c ≥ 7 %. Of the 90 patients, 38 (42.2 %) presented with coronary atherosclerotic plaques, 11 had A1c < 7 % and 27 had A1c ≥ 7 % (p = 0.0006). Fourteen patients had significant lumen obstruction higher than 50 %: 3 in the A1c < 7 % group and 11 in the A1c ≥ 7 % group (p = 0.02). Non-calcified plaque was more prevalent in the A1c ≥ 7 % group (p = 0.005). In eleven patients, the simultaneous presence of two vulnerability plaque characteristics (PR and LAP) were observed more frequently in the A1c ≥ 7 group (n = 8) than in the A1c < 7 group (n = 3) (p = 0.04). Asymptomatic DM2 patients with A1c ≥ 7 % have a higher frequency of CAD and a higher proportion of vulnerable atherosclerotic coronary plaque by MDCT compared to patients with DM2 with A1c < 7 in our study.

Relation between Gd-DTPA contrast enhancement and regional inotropic response in the periphery and center of myocardial infarction.

BACKGROUND: Gd-DTPA contrast-enhanced (CE) MRI identifies patterns of early hypoenhancement and delayed hyperenhancement in acute myocardial infarction, but their clinical significance for the prediction of myocardial viability remains controversial. Therefore, we closely examined the relationship between these CE patterns and regional inotropic response to low-dose dobutamine infusion at a regional level. METHODS AND RESULTS: Thirteen dogs underwent CE and tagged MRI at rest and during 5 microg. kg(-1). min(-1) dobutamine 48 hours after MI. CE patterns and 3D regional strains were measured in 96 segments per animal. Segments were categorized as being normofunctional (n=828) if resting circumferential shortening was within the range of remote myocardium, or dysfunctional (n=420) if not. Inotropic response in resting dysfunctional segments was assessed according to CE patterns. Significant improvement of radial thickening (from +12+/-1% [mean+/-SEM] to +22+/-2%, P<0.05) and circumferential shortening (from +1+/-1% to -5+/-1%, P<0.05) strains occurred in dysfunctional myocardium with normal CE pattern but not in myocardium with early hypoenhancement. Delayed hyperenhanced myocardium displayed a more complex behavior. Circumferential stretching improved in the peripheral regions (from +4+/-1% to -2+/-2%, P<0.05), where the infarct was nontransmural (38+/-3% transmurality), but not in centrally hyperenhanced regions (from +4+/-1% to +1+/-1% P=NS), where the infarct was 66+/-3% transmural. CONCLUSIONS: Inotropic reserve was confined to dysfunctional myocardium with normal contrast enhancement but not to myocardium with early hypoenhancement. Inotropic response in delayed hyperenhanced myocardium is influenced by transmurality of necrosis. These observations support the use of CE MRI for the clinical detection of myocardial viability.

Microvascular obstruction and left ventricular remodeling early after acute myocardial infarction.

BACKGROUND: The presence of microvascular obstruction (MO) within infarcted regions may adversely influence left ventricular (LV) remodeling after acute myocardial infarction. This study examined whether the extent of MO directly alters the mechanical properties of the infarcted myocardium. METHODS AND RESULTS: Seventeen dogs underwent 90 minutes of balloon occlusion of the left anterior descending coronary artery, followed by reperfusion. Gadolinium-enhanced perfusion MRI and 3D-tagging were performed 4 to 6 and 48 hours (8 animals) and 10 days (9 animals) after reperfusion. Early increase in LV end-diastolic volume (from 42+/-9 to 54+/-14 mL, P<0.05) between 4 to 6 and 48 hours after reperfusion was predicted by both extent of MO (r=0.89, P<0.01) and infarct size (r=0.83, P<0.01), defined as MRI hypoenhanced and hyperenhanced regions, respectively. Multivariate analysis demonstrated that extent of MO had better and independent value to predict LV volume than overall infarct size. A strong inverse relationship existed between magnitude of first principal strain (r=-0.80, P<0.001) and relative extent of MO within infarcted myocardium. Also, infarcted myocardium involved by extensive areas of MO demonstrated reductions of circumferential (r=-0.61, P<0.01) and longitudinal (r=-0.53, P<0. 05) stretching. Furthermore, significant reductions of radial thickening (9+/-6% versus 14+/-3%, P<0.01) occurred in noninfarcted regions adjacent to infarcts that had increased (>35%) amounts of MO. CONCLUSIONS: In the early healing phase of acute myocardial infarction, the extent of MO in infarcted tissue relates to reduced local myocardial deformation and dysfunction of noninfarcted adjacent myocardium. Such strain alterations might explain the increased remodeling observed in patients with large regions of MO.

Fast determination of regional myocardial strain fields from tagged cardiac images using harmonic phase MRI.

BACKGROUND: Tagged MRI of the heart is difficult to implement clinically because of the lack of fast analytical techniques. We investigated the accuracy of harmonic phase (HARP) imaging for rapid quantification of myocardial strains and for detailed analysis of left ventricular (LV) function during dobutamine stimulation. METHODS AND RESULTS: Tagged MRI was performed in 10 volunteers at rest and during 5 to 20 microg(-1). kg(-1). min(-1) dobutamine and in 9 postinfarct patients at rest. We compared 2D myocardial strains (circumferential shortening, Ecc; maximal shortening, E(2); and E(2), direction) as assessed by a conventional technique and by HARP. Full quantitative analysis of the data was 10 times faster with HARP. For pooled data, the regression coefficient was r=0.93 for each strain (P<0.001). In volunteers, Ecc and E(2) were greater in the free wall than in the septum (P<0.01), but recruitable myocardial strain at peak dobutamine was greater in the LV septum (P<0.01). E(2) orientation shifted away from the circumferential direction at peak dobutamine (P<0.01). HARP accurately detected subtle changes in myocardial strain fields under increasing doses of dobutamine. In patients, HARP-determined Ecc and E(2) values were dramatically reduced in the asynergic segments as compared with remote (P<0.001), and E(2) direction shifted away from the circumferential direction (P<0.001). CONCLUSIONS: HARP MRI provides fast, accurate assessment of myocardial strains from tagged MR images in normal subjects and in patients with coronary artery disease with wall motion abnormalities. HARP correctly indexes dobutamine-induced changes in strains and has the potential for on-line quantitative monitoring of LV function during stress testing.

Ventricular pacing with premature excitation for treatment of hypertensive-cardiac hypertrophy with cavity-obliteration.

BACKGROUND: Hypertensive left ventricular hypertrophy with supranormal systolic ejection and distal cavity obliteration (HHCO) can result in debilitating exertional fatigue and dyspnea. Dual-chamber pacing with ventricular preactivation generates discoordinate contraction, which can limit cavity obliteration and thereby increase potential ejection reserve. Accordingly, we hypothesized that pacing may improve exercise tolerance long-term in this syndrome. METHODS AND RESULTS: Dual-chamber pacemakers were implanted in 9 patients with exertional dyspnea caused by HHCO. Intrinsic atrial rate was sensed, and ventricular preactivation was achieved by shortening the atrial-ventricular delay. Pacing was on or off for successive 3-month periods (randomized, double-blind, crossover design), followed by 6 additional pacing-on months. Metabolic exercise testing, quality-of-life assessment, and rest and dobutamine-stress echocardiographic/Doppler data were obtained. After 3 months of pacing-on, exercise duration rose from 324+/-133 to 588+/-238 s (mean+/-SD; P=0.001, with 7 of 9 patients improving >/=30%), and maximal oxygen consumption increased from 13.6+/-2.9 to 16.7+/-3.3 mL of O(2). min(-1). kg(-1) (P<0.02). Both parameters were little changed from baseline during the pacing-off period. Improved exercise capacity persisted at 1-year follow-up. Clinical symptoms and activities of daily living improved during the pacing-on period and stayed improved at 1 year, but they were little changed during the pacing-off period. Despite similar basal values, stroke volume (P<0.001) and cardiac output (P<0.02) increased with dobutamine stimulation 2 to 3 times more after 1 year of follow-up as compared with baseline. CONCLUSIONS: Long-term dual-chamber pacing can improve exercise capacity, cardiac reserve, clinical symptoms, and activities of daily living in patients with HHCO. This therapy may provide a novel alternative for patients in whom traditional pharmacological treatment proves inadequate.

Transmural contractile reserve after reperfused myocardial infarction in dogs.

OBJECTIVES: The goal of this study was to characterize detailed transmural left ventricular (LV) function at rest and during dobutamine stimulation in subendocardial and transmural experimental infarcts. BACKGROUND: The relation between segmental LV function and the transmural extent of myocardial necrosis is complex. However, its detailed understanding is crucial for the diagnosis of myocardial viability as assessed by inotropic stimulation. METHODS: Short-axis tagged magnetic resonance images were acquired at five to seven levels encompassing the LV from base to apex in seven dogs 2 days after a 90-min closed-chest left anterior descending coronary occlusion, followed by reflow. Myocardial strains were measured transmurally in the entire LV by harmonic phase imaging at rest and 5 ig x kg(-1) x min(-1) dobutamine. Risk regions were assessed by radioactive microspheres, and the transmural extent of the infarct was assessed by 2,3,5 triphenyltetrazolium chloride staining. RESULTS: Circumferential shortening (Ecc), radial thickening (Err) and maximal shortening at rest were greater in segments with subendocardial versus transmural infarcts, both in subepicardium (-1.1+/-1.0 vs. 2.5+/-0.6% for Ecc, -0.5+/-1.9 vs. -1.8+/-1.0% for Err, p < 0.05) and subendocardium (-2.0+/-1.4 vs. 2.8+/-0.8%, 2.4+/-1.7 vs. 0.0+/-0.9%, respectively, p < 0.05). Under inotropic stimulation, risk regions retained maximal contractile reserve. Recruitable deformation was found in outer layers of subendocardial infarcts (p < 0.01 for Ecc and Err) but also in inner layers (p < 0.01). Conversely, no contractile reserve was observed in segments with transmural infarcts. CONCLUSIONS: Under dobutamine challenge, recruitment of myofiber shortening and thickening was observed in inner layers of segments with subendocardial infarcts. These results may have important clinical implications for the detection of myocardial viability.

Noninvasive single-beat determination of left ventricular end-systolic elastance in humans.

OBJECTIVES: The goal of this study was to develop and validate a method to estimate left ventricular end-systolic elastance (E(es)) in humans from noninvasive single-beat parameters. BACKGROUND: Left ventricular end-systolic elastance is a major determinant of cardiac systolic function and ventricular-arterial interaction. However, its use in heart failure assessment and management is limited by lack of a simple means to measure it noninvasively. This study presents a new noninvasive method and validates it against invasively measured E(es). METHODS: Left ventricular end-systolic elastance was calculated by a modified single-beat method employing systolic (P(s)) and diastolic (P(d)) arm-cuff pressures, echo-Doppler stroke volume (SV), echo-derived ejection fraction (EF) and an estimated normalized ventricular elastance at arterial end-diastole (E(Nd)): E(es(sb)) = [P(d) - (E(Nd(est)) x P(s) x 0.9)[/(E(Nd(est)) x SV). The E(Nd) was estimated from a group-averaged value adjusted for individual contractile/loading effects; E(es(sb)) estimates were compared with invasively measured values in 43 patients with varying cardiovascular disorders, with additional data recorded after inotropic stimulation (n = 18, dobutamine 5 to 10 microg/kg per min). Investigators performing noninvasive analysis were blinded to the invasive results. RESULTS: Combined baseline and dobutamine-stimulated E(es) ranged 0.4 to 8.4 mm Hg/ml and was well predicted by E(es(sb)) over the full range: E(es) = 0.86 x E(es(sb)) + 0.40 (r = 0.91, SEE = 0.64, p < 0.00001, n = 72). Absolute change in E(es(sb)) before and after dobutamine also correlated well with invasive measures: E(es(sb)): DeltaE(es) = 0.86 x DeltaE(es(sb)) + 0.67 (r = 0.88, p < 0.00001). Repeated measures of E(es(sb)) over two months in a separate group of patients (n = 7) yielded a coefficient of variation of 20.3 +/- 6%. CONCLUSIONS: The E(es) can be reliably estimated from simple noninvasive measurements. This approach should broaden the clinical applicability of this useful parameter for assessing systolic function, therapeutic response and ventricular-arterial interaction.

Quantification and time course of microvascular obstruction by contrast-enhanced echocardiography and magnetic resonance imaging following acute myocardial infarction and reperfusion.

OBJECTIVES: We aimed to validate contrast-enhanced echocardiography (CE) in the quantification of microvascular obstruction (MO) against magnetic resonance imaging (MRI) and the histopathologic standards of radioactive microspheres and thioflavin-S staining. We also determined the time course of MO at days 2 and 9 after infarction and reperfusion. BACKGROUND: Postinfarction MO occurs because prolonged ischemia produces microvessel occlusion at the infarct core, preventing adequate reperfusion. Microvascular obstruction expands up to 48 h after reperfusion; the time course beyond 2 days is unknown. Though used to study MO, CE has not been compared with MRI and thioflavin-S, which yield precise visual maps of MO. METHODS: Ten closed-chest dogs underwent 90-min coronary artery occlusion and reperfusion. Both CE and MRI were performed at 2 and 9 days after reperfusion. The MO regions by both methods were quantified as percent left ventricular (% LV) mass. Radioactive microspheres were injected for blood flow determination. Postmortem, the myocardium was stained with thioflavin-S and 2,3,5-triphenyltetrazolium chloride. RESULTS: Expressed as % total LV, MO by MRI matched in size MO by microspheres using a flow threshold of <40% remote (4.96+/-3.52% vs. 5.32+/-3.98%, p=NS). For matched LV cross sections, MO by CE matched in size MO by microspheres using a flow threshold of <60% remote (13.27+/-4.31% vs. 13.5+/-4.94%, p=NS). Both noninvasive techniques correlated well with microspheres (MRI vs. CE, r=0.87 vs. 0.74; p=NS). Microvascular obstruction by CE corresponded spatially to MRI-hypoenhanced regions and thioflavin-negative regions. For matched LV slices at 9 days after reperfusion, MO measured 12.94+/-4.51% by CE, 7.11+/-3.68% by MRI and 9.18+/-4.32% by thioflavin-S. Compared to thioflavin-S, both noninvasive techniques correlated well (CE vs. MRI, r=0.79 vs. 0.91; p=NS). Microvascular obstruction size was unchanged at 2 and 9 days (CE: 13.23+/-4.11% vs. 12.69+/-4.97%; MRI: 5.53+/-4.94% vs. 4.68+/-3.44%; p=NS for both). CONCLUSIONS: Both CE and MRI can quantify MO. Both correlate well with the histopathologic standards. While MRI can detect regions of MO with blood flow <40% of remote, the threshold for MO by CE is <60% remote. The extent of MO is unchanged at 2 and 9 days after reperfusion.

Compensatory enlargement of human coronary arteries identified by magnetic resonance imaging.

The aim of the present study was to evaluate the role of magnetic resonance imaging (MRI) for the non-invasive detection of coronary abnormalities and specifically the remodeling process in patients with coronary artery disease (CAD). MRI was performed in 10 control healthy subjects and 26 patients with angiographically proven CAD of the right coronary (RCA) or left anterior descending (LAD) artery; 23 patients were within two months of acute coronary syndromes, and 3 had stable angina with a positive test for ischemia. Wall thickness (WT), vessel wall area (VWA), total vessel area (TVA), and luminal area (LA) were measured. There were significant increases in WT (mean +/- SEM, RCA: 2.62 +/- 0.75 vs 0.53 +/- 0.15 mm; LAD: 2.21 +/- 0.69 vs 0.62 +/- 0.24 mm) and in VWA (RCA: 30.96 +/- 17.57 vs 2.1 +/- 1.2 mm(2); LAD: 19.53 +/- 7.25 vs 3.6 +/- 2.0 mm(2)) patients compared to controls (P < 0.001 for each variable). TVA values were also greater in patients compared to controls (RCA: 44.56 +/- 21.87 vs 12.3 +/- 4.2 mm(2); LAD: 31.89 +/- 11.31 vs 17.0 +/- 6.2 mm(2); P < 0.001). In contrast, the LA did not differ between patients and controls for RCA or LAD. When the LA was adjusted for vessel size using the LA/TVA ratio, a significant difference was found: 0.33 +/- 0.16 in patients vs 0.82 +/- 0.09 in controls (RCA) and 0.38 +/- 0.13 vs 0.78 +/- 0.06 (LAD) (P < 0.001). As opposed to normal controls, positive remodeling was present in all patients with CAD, as indicated by larger VWA. We conclude that MRI detected vessel wall abnormalities and was an effective tool for the noninvasive evaluation of the atherosclerotic process and coronary vessel wall modifications, including positive remodeling that frequently occurs in patients with acute coronary syndromes.

Usefulness of ST-segment depression in non-infarct-related electrocardiographic leads in predicting prognosis after thrombolytic therapy for acute myocardial infarction.

This study investigated both the in-hospital and long-term prognostic significance of ST-segment depression in non-infarct-related leads in patients who received thrombolytic therapy after acute myocardial infarction (AMI). We evaluated 221 consecutive patients who were admitted with their first AMI and underwent thrombolysis. Patients were followed for an average of 31 months and were classified into 3 groups: group 1 included 51 patients with persistent ST-segment depression, group 2 had 97 patients with transient ST-segment depression, and group 3 consisted of 73 patients without ST-segment depression (absent). Group 1 had significantly worse long-term survival during follow up by Kaplan-Meier analysis (55%) versus group 2 (81%) and group 3 (94%) (p = 0.0004) and higher event rates. This prognostic significance seemed to be maintained in both the anterior and inferior wall AMI groups. Multivariate analysis, using the Cox model, showed that Killip class, in-hospital left ventricular ejection fraction, and the persistence of ST-segment depression on the predischarge electrocardiogram (group 1) were independent predictors of survival. ST-segment depression in non-infarct-related leads on the predischarge electrocardiogram is an independent risk factor for worse long-term survival after anterior as well as inferior AMI treated with thrombolytic therapy.

Enhancement of contrast echocardiography by image variability analysis.

BACKGROUND: Although there have been recent advances in echocardiography, many studies remain suboptimal due to poor image quality and unclear blood-myocardium border. We developed a novel image processing technique, cardiac variability imaging (CVI), based on the variance of pixel intensity values during passage of ultrasound microbubble contrast into the left ventricle chamber, with the aim of enhancing endocardial border delineation and image quality. METHODS AND RESULTS: CVI analysis was performed on simulated data to test and verify the mechanism of image enhancement. Then CVI analysis was applied to echocardiographic images obtained in two different clinical studies, and still images were interpreted by expert reviewers. In the first study (N = 15), using contrast agent EchoGen, the number of observable wall segments in end-diastolic images, for example, was significantly increased by CVI (4.93) as compared to precontrast (3.28) and contrast images (3.36), P < 0.001 for both comparisons to CVI. In the second study (N = 8), using contrast agent Optison, interobserver variability of manually traced end-diastolic volumes was significantly decreased using CVI (22.3 ml) as compared to precontrast (63.4) and contrast images (49.0), P < 0.01 for both comparisons to CVI. CONCLUSION: CVI can substantially enhance endocardial border delineation and improve echocardiographic image quality and image interpretation.

Case report: MRI evaluation of congenital coronary artery fistulae.

Congenital coronary artery fistula is a rare disease and MRI is a promising technique that may be useful to demonstrate the coronary artery tree. We report three patients who underwent cardiac MRI to investigate right coronary artery fistulae. On clinical examination, a continuous murmur was heard along the left sternal border, and chest X-ray showed moderate cardiomegaly with enlargement of right chambers in all patients. Transthoracic Doppler echocardiography showed fistulae in two cases; the third case was not demonstrated by transthoracic or transoesophageal echocardiography. MRI demonstrated the course of the fistulous vessels in all patients. All patients underwent surgical closure of their coronary artery fistulae. MRI may show detailed anatomy of congenital coronary artery fistulae and may be useful as an additional non-invasive method in their investigation.

[Role of circumflex coronary artery involvement in non-Q wave myocardial infarction]. / Papel do acometimento da artéria coronária circunflexa no infarto do miocárdio sem onda Q.

PURPOSE: To determine the patency and incidence rates of left circumflex coronary artery (LCX) as the infarct related artery (IRA) in Q-wave and non-Q wave acute myocardial infarction (AMI). METHODS: Two-hundreds and twenty one patients (172 men) with AMI were stratified in Q and non-Q waves groups. All patients were submitted to cinecoronary angiography 72 hours after the beginning of symptoms and the IRA and its patency were evaluated. RESULTS: In non-Q wave AMI, the LCX was considered to be the IRA in 35% of the patients. In Q wave AMI, this incidence was 8% (p < 0.001). Occlusion of LCX was seen in all non-Q wave AMI patients when it was the IRA. CONCLUSION: The incidence of LCX as IRA was significantly higher in non-Q wave AMI patients. This group did not have the previously expected greater patency rates, what could result in different clinical and evolutive characteristics.

[Hospital outcome of patients with right ventricular infarction and the importance of right coronary artery patency]. / Evolução hospitalar de pacientes com infarto de ventrículo direito e a importância da perviabilidade da artéria coronária direita.

PURPOSE: To evaluate the importance of the right coronary artery (RCA) patency in patients with right ventricular infarction. METHODS: Fifty-two patients with inferior wall myocardial infarction and right ventricular involvement were studied and divided in two groups: group A (GA) included 35 patients in whom the RCA was patent at coronary angiography, and group B (GB), 17 who had an occluded RCA. They were prospectively evaluated for electrical and hemodynamic complications, as well as in-hospital mortality. RESULTS: The mortality in GA was 11% and 29% in GB, p = 0.13; electrical complications were 11% in GA and 35% in GB, p = 0.06; hemodynamic complications were 8% in GA and 41% in GB, p = 0.009. CONCLUSION: These findings suggest a trend towards reduction in mortality and electrical complications, and significant reduction of hemodynamic complications in patients with inferior wall myocardial infarction with involvement of the right ventricle who have the RCA patent. Thus, RCA patency appears to be important in determining in-hospital outcomes of these patients.

Coronary artery plaque burden and calcium scores in healthy men adhering to long-term wine drinking or alcohol abstinence.

Observational studies suggest there are clinical benefits to moderate red wine (RW) consumption. However, the effects on coronary vasculature and overall lifestyle are unclear. We investigated whether a lifestyle of regular long-term RW consumption is associated with changes in coronary plaque burden, calcium score, carotid intima/media thickness, endothelial function, and metabolic variables, compared with alcohol abstinence. Healthy volunteers were evaluated by coronary computed tomography angiography (CTA) as well as carotid and brachial artery ultrasound. Nutritional status, psychological status, and metabolic variables were assessed. The study included 101 drinkers [aged 58.9 ± 7.3 years (means ± SD)], from wine brotherhoods, and 104 abstainers, from Anglican, Evangelical and Catholic churches both in the city of São Paulo, Brazil. No significant differences in demographics were noted. Lesion prevalence per patient assessed by coronary CTA and classified as absent (0), 1-25, 26-49, and ≥ 50% stenosis was similar between groups. When analyzed by individual arteries, i.e., left anterior descending, circumflex, and right coronary, prevalence was also not different. On the other hand, calcium scores were higher among drinkers than abstainers (144.4 ± 362.2 vs 122.0 ± 370.3; P<0.01). However, drinkers reported less history of diabetes and exercised more. RW drinkers consumed 2127.9 ± 387.7 kcal/day while abstainers consumed 1836.0 ± 305.0 (P<0.0001). HDL cholesterol was significantly higher among drinkers compared to abstainers (46.9 ± 10.9 vs 39.5 ± 9.0 mg/dL; P<0.001), while fasting plasma glucose was lower (97.6 ± 18.2 vs 118.4 ± 29.6 mg/dL; P<0.02). Liver enzymes were normal in both groups. In conclusion, long-term wine drinkers displayed a similar plaque burden but greater calcium score than abstainers, despite a more atherogenic diet, and the mechanisms for the increased calcium scores in the former remain speculative.

Red wine consumption, coronary calcification, and long-term clinical evolution

Coronary artery calcification (CAC) is associated with atherosclerotic complications. However, elevated CAC may not always imply a worse prognosis. Herein, we report the clinical evolution of long-term red wine (RW) drinkers in relation to CAC. We followed 200 healthy male habitual RW drinkers and compared them to 154 abstainers for a period of 5.5 years. The initial evaluation included coronary computed tomography angiography (CTA), clinical, demographics, and laboratory data. CAC was quantified by the Agatston score. The follow-up process was conducted by telephone calls and/or hospital record review. The composite end-point of total death, acute myocardial infarction (AMI), or coronary revascularization (or major adverse cardiac event - MACE) was assessed. The RW drinkers ingested 28.9±15 g of alcohol/day for 23.4±12.3 years. They had higher high-density lipoprotein and low-density lipoprotein, but lower C-reactive protein than abstainers. Age, total cholesterol, triglycerides, glucose, and liver enzymes were similar. History of diabetes was lower among drinkers, but other risk factors were similar. However, drinkers had higher CAC than abstainers; the mean value was 131.5±362 in drinkers vs 40.5±320 in abstainers (P<0.001). The median and interquartile range were 15 (0.0-131.5) in RW drinkers and 1 (0.0-40.5) in abstainers (P=0.003). During the follow-up, MACE was significantly lower in drinkers than in abstainers, despite their higher CAC. The difference was driven mainly by AMI (0 vs 6; P<0.03). Greater CAC values in this setting did not predict worse prognosis. A possible underlying mechanism is lesion calcification, which leads to plaque stabilization and less clinical events.