Early identification of asymptomatic subjects at increased risk of heart failure and cardiovascular events: progress and future directions.

Increasing evidence for a latent, preclinical phase of cardiac pathology prior to the development of symptomatic heart failure has fuelled interest in the potential of developing a screening program for early disease detection and intervention. Cardiac biomarkers have shown promise in identifying subjects with significant left ventricular dysfunction and more recently to assist in cardiovascular risk stratification. However, a number of questions remain regarding the use of these biomarkers for screening purposes. In particular, appropriate cut-off levels and adjustment for individual patient characteristics still need to be established and further cost-effectiveness studies are required before screening programs can be undertaken. Given the enormous and increasing burden of cardiac failure worldwide, the potential of these biomarkers to identify those at greatest risk of the condition, either alone or as part of a hybrid screening strategy is of great interest to the cardiology community. The aim of this review is to outline evidence behind the argument for screening, discuss the remaining barriers to its development and implementation and highlight potential areas for future research.

Most individuals with treated blood pressures above target receive only one or two antihypertensive drug classes.

BACKGROUND: A significant proportion of individuals taking antihypertensive therapies fail to achieve blood pressures <140/90 mmHg. In order to develop strategies for improved treatment of blood pressure, we examined the association of blood pressure control with antihypertensive therapies and clinical and lifestyle factors in a cohort of adults at increased cardiovascular risk. METHODS: A cross-sectional study of 3994 adults from Melbourne and Shepparton, Australia enrolled in the SCReening Evaluation of the Evolution of New Heart Failure (SCREEN-HF) study. Inclusion criteria were age ≥60 years with one or more of self-reported ischaemic or other heart disease, atrial fibrillation, cerebrovascular disease, renal impairment or treatment for hypertension or diabetes for ≥2 years. Exclusion criteria were known heart failure or cardiac abnormality on echocardiography or other imaging. The main outcome measures were the proportion of participants receiving antihypertensive therapy with blood pressures ≥140/90 mmHg and the association of blood pressure control with antihypertensive therapies and clinical and lifestyle factors. RESULTS: Of 3623 participants (1975 men and 1648 women) receiving antihypertensive therapy, 1867 (52%) had blood pressures ≥140/90 mmHg. Of these 1867 participants, 1483 (79%) were receiving only one or two antihypertensive drug classes. Blood pressures ≥140/90 mmHg were associated with increased age, male sex, waist circumference and log amino-terminal-pro-B-type natriuretic peptide levels. CONCLUSIONS: Most individuals with treated blood pressures above target receive only one or two antihypertensive drug classes. Prescribing additional antihypertensive drug classes and lifestyle modification may improve blood pressure control in this population of individuals at increased cardiovascular risk.

Acute rheumatic fever and rheumatic heart disease--priorities in prevention, diagnosis and management. A report of the CSANZ Indigenous Cardiovascular Health Conference, Alice Springs 2011.

Three priority areas in the prevention, diagnosis and management of acute rheumatic fever (ARF) and rheumatic heart disease (RHD) were identified and discussed in detail: 1. Echocardiography and screening/diagnosis of RHD ­ Given the existing uncertainty it remains premature to advocate for or to incorporate echocardiographic screening for RHD into Australian clinical practice. Further research is currently being undertaken to evaluate the potential for echocardiography screening. 2. Secondary prophylaxis ­ Secondary prophylaxis (long acting benzathine penicillin injections) must be seen as a priority. Systems-based approaches are necessary with a focus on the development and evaluation of primary health care-based or led strategies incorporating effective health information management systems. Better/novel systems of delivery of prophylactic medications should be investigated. 3. Management of advanced RHD ­ National centres of excellence for the diagnosis, assessment and surgical management of RHD are required. Early referral for surgical input is necessary with multidisciplinary care and team-based decision making that includes patient, family, and local health providers. There is a need for a national RHD surgical register and research strategy for the assessment, intervention and long-term outcome of surgery and other interventions for RHD.

Increased tissue kallikrein levels in type 2 diabetes.

AIMS/HYPOTHESIS: We measured components of the kallikrein- kinin system in human type 2 diabetes mellitus and the effects of statin therapy on the circulating kallikrein-kinin system. METHODS: Circulating levels of bradykinin and kallidin peptides, and high and low molecular weight kininogens, as well as plasma and tissue kallikrein, and kallistatin were measured in non-diabetic and diabetic patients before coronary artery bypass graft surgery. Tissue kallikrein levels in atrial tissue were examined by immunohistochemistry and atrial tissue kallikrein mRNA quantified. RESULTS: Plasma levels of tissue kallikrein were approximately 62% higher in diabetic than in non-diabetic patients (p=0.001), whereas no differences were seen in circulating levels of bradykinin and kallidin peptides, and high and low molecular weight kininogens, or in plasma kallikrein or kallistatin. Immunohistochemistry revealed a twofold increase in tissue kallikrein levels in atrial myocytes (p= 0.015), while tissue kallikrein mRNA levels were increased eightfold in atrial tissue of diabetic patients (p=0.014). Statin therapy did not change any variables of the circulating kallikrein-kinin system. Neither aspirin, calcium antagonists, beta blockers or long-acting nitrate therapies influenced any kallikrein-kinin system variable. CONCLUSIONS/INTERPRETATION: Tissue kallikrein levels are increased in type 2 diabetes, whereas statin therapy does not modify the circulating kallikrein-kinin system. Cardiac tissue kallikrein may play a greater cardioprotective role in type 2 diabetic than in non-diabetic patients and contribute to the benefits of ACE inhibitor therapy in type 2 diabetic patients. However, our findings do not support a role for the kallikrein-kinin system in mediating the effects of statin therapy on endothelial function.

Biochemical and functional abnormalities of left and right ventricular function after ultra-endurance exercise.

BACKGROUND: There is evidence that ultra-endurance exercise causes myocardial injury. The extent and duration of these changes remains unresolved. Recent reports have speculated that structural adaptations to exercise, particularly of the right ventricle, may predispose to tachyarrhythmias and sudden cardiac death. OBJECTIVE: To quantify the extent and duration of post-exercise cardiac injury with particular attention to right ventricular (RV) dysfunction. METHODS: 27 athletes (20 male, 7 female) were tested 1 week before, immediately after and 1 week after an ultra-endurance triathlon. Tests included cardiac troponin I (cTnI), B-type natriuretic peptide (BNP) and comprehensive echocardiographic assessment. RESULTS: 26 athletes completed the race and testing procedures. Post-race, cTnI was raised in 15 athletes (58%) and the mean value for the entire cohort increased (0.17 vs 0.49 microg/l, p<0.01). BNP rose in every athlete and the mean increased significantly (12.2 vs 42.5 ng/l, p<0.001). Left ventricular ejection fraction (LVEF) was unchanged (60.4% vs 57.5%, p = 0.09), but integrated systolic strain decreased (16.9% vs 15.1%, p<0.01). New regional wall motion abnormalities developed in seven athletes (27%) and LVEF was reduced in this subgroup (57.8% vs 45.9%, p<0.001). RV function was reduced in the entire cohort with decreases in fractional area change (0.47 vs 0.39, p<0.01) and tricuspid annular plane systolic excursion (21.8 vs 19.1 mm, p<0.01). At follow-up, all variables returned to baseline except in one athlete where RV dysfunction persisted. CONCLUSION: Myocardial damage occurs during intense ultra-endurance exercise and, in particular, there is a significant reduction in RV function. Almost all abnormalities resolve within 1 week.

Functional, structural and molecular aspects of diastolic heart failure in the diabetic (mRen-2)27 rat.

OBJECTIVE: Diabetic cardiomyopathy is an increasingly recognized cause of cardiac failure despite preserved left ventricular systolic function. Given the over-expression of angiotensin II in human diabetic cardiomyopathy, we hypothesized that combining hyperglycaemia with an enhanced tissue renin-angiotensin system would lead to the development of diastolic dysfunction with adverse remodeling in a rodent model. METHODS: Homozygous (mRen-2)27 rats and non-transgenic Sprague Dawley (SD) rats were randomized to receive streptozotocin (diabetic) or vehicle (non-diabetic) and followed for 6 weeks. Prior to tissue collection, animals underwent pressure-volume loop acquisition. RESULTS: Diabetic Ren-2 rats developed impairment of both active and passive phases of diastole, accompanied by reductions in SERCA-2a ATPase and phospholamban along with activation of the fetal gene program. Structural features of diabetic cardiomyopathy in the Ren-2 rat included interstitial fibrosis, cardiac myocyte hypertrophy and apoptosis in conjunction with increased activity of transforming growth factor-beta (p<0.01 compared with non-diabetic Ren-2 rats for all parameters). No significant functional or structural derangements were observed in non-transgenic, SD diabetic rats. CONCLUSION: These findings indicate that the combination of enhanced tissue renin-angiotensin system and hyperglycaemia lead to the development of diabetic cardiomyopathy. Fibrosis, and myocyte hypertrophy, a prominent feature of this model, may be a consequence of activation of the pro-sclerotic cytokine, transforming growth factor-beta, by the diabetic state.

Traditional risk factor assessment does not capture the extent of cardiovascular risk in systemic lupus erythematosus.

BACKGROUND: Systemic lupus erythematosus (SLE) is associated with accelerated atherosclerosis. However, the degree of endothelial dysfunction and its relationship to traditional and novel cardiovascular risk factors have not been examined in SLE. METHODS: In a case-control design, 35 patients with clinically stable SLE and 35 control subjects matched for age, sex, body mass index and smoking status were studied. Arterial elasticity, lipid profile, homocysteine, measures of inflammation and oxidative stress were determined. RESULTS: Among traditional vascular risk factors, there was a nonsignificant trend towards lower blood pressure in the control subjects, whereas low-density lipoprotein (LDL) cholesterol levels were significantly lower in the SLE group (2.5 vs 3.3 mmol/L, P < 0.001). Patients with SLE had significantly lower small artery elasticity (SAE; 4.9 vs 7.0 ml/mmHg x 100, P < 0.001) and higher plasma homocysteine (11.4 vs 8.3 mmol/L, P = 0.002) than control subjects. Levels of serum sVCAM-1 (614 vs 494 ng/mL, P = 0.002), oxidized LDL (144 vs 97, P < 0.001) and CD40 ligand (4385 vs 1373 pg/ml, P = 0.001) were significantly higher in SLE. Oxidized LDL levels, older age at SLE diagnosis and higher disease damage scores correlated inversely with SAE but not traditional risk factors. CONCLUSION: Impaired endothelial function as shown by decreased SAE, and an adverse profile of novel proatherogenic and prothrombotic vascular disease risk factors were prevalent in clinically quiescent SLE. These findings show the vulnerability of patients with SLE for atherosclerosis, and emphasize that assessments based on traditional risk factors alone may be inadequate.

Load-sensitive measures may overestimate global systolic function in the presence of left ventricular hypertrophy: a comparison with load-insensitive measures.

Transgenic animal models have provided a vital insight into the pathogenesis of cardiovascular disease, but functional cardiac assessment is often limited by high heart rates and small heart size. We hypothesized that in the presence of concentric left ventricular (LV) hypertrophy (LVH), load-sensitive measures of contractility may be misinterpreted as overestimating global cardiac function, because the normal function of excess sarcomeres may displace a greater volume of blood during contraction. Conductance catheter technology was used to evaluate pressure-volume (P-V) relationships as a load-insensitive method of assessing cardiac function in vivo in 18-wk-old heterozygous (mRen-2)27 transgenic rats (a model of LVH), compared with age-matched Sprague-Dawley (SD) controls. Anesthetized animals underwent echocardiography followed by P-V loop analysis. Blood pressure, body weight, and heart rate were higher in the Ren-2 rats (P < 0.05). Load-sensitive measures of systolic function, including fractional area change, fractional shortening, ejection fraction, and positive peak rate of LV pressure development, were greater in the Ren-2 than control animals (P < 0.05). Load-insensitive measures of systolic function, including the preload recruitable stroke work relationship and the end-systolic P-V relationship, were not different between Ren-2 and SD rats. Regional wall motion assessed by circumferential shortening velocity suggested enhanced circumferential fiber contractility in the Ren-2 rats (P = 0.02), but tissue Doppler imaging, used to assess longitudinal function, was not different between groups. Although conventional measures suggested enhanced systolic function in the Ren-2 rat, load-insensitive measures of contractility were not different between Ren-2 and SD animals. These findings suggest that the normal range of values for load-sensitive indexes of contractility needs to be altered according to the degree of LVH. To accurately identify changes in systolic function, we suggest that a combination of echocardiography with assessment of load-insensitive measures be used routinely.

No evidence of sustained myocardial injury following an Ironman distance triathlon.

We aimed to determine whether an Ironman distance triathlon resulted in sustained myocardial injury detected by electrocardiography, biochemical markers or echocardiographic assessment of left ventricular systolic and diastolic function. Electrocardiograms, blood for analysis of creatine kinase (CK) and its MB fraction, cardiac troponin I (cTnI) and echocardiograms were obtained in 15 male athletes prior to and at a mean of 4.7 days after competing in the Australian Ironman Triathlon. Regional wall motion scores, left ventricular ejection fraction (LVEF) and mitral inflow parameters were determined from the echocardiograms by a blinded investigator. Levels of cTnI were undetectable in all athletes and total CK was mildly elevated in 7/15 athletes prior to the event. Baseline wall motion, ejection fraction and diastolic filling were normal in all athletes. CK levels were increased post-race (p < 0.05) with a mean post-race level of 451U/l. Levels of cTnI were undetectable post-race in 14 athletes with a level of 0.9 microg/l recorded in one athlete, although all were within the laboratory's normal range for the assay. Mitral inflow parameters and LVEF did not change post-race and regional wall motion was normal in 14 of 15 athletes. Regional wall motion abnormalities detected in 1 athlete had resolved by 25 days post-race. These findings indicate that ultraendurance exercise does not result in sustained myocardial injury in this group of elite athletes.

Interaliasing distance of the flow convergence surface for determining mitral regurgitant volume: a validation study in a chronic animal model.

OBJECTIVES: We aimed to validate a new flow convergence (FC) method that eliminated the need to locate the regurgitant orifice and that could be performed semiautomatedly. BACKGROUND: Complex and time-consuming features of previously validated color Doppler methods for determining mitral regurgitant volume (MRV) have prevented their widespread clinical use. METHODS: Thirty-nine different hemodynamic conditions in 12 sheep with surgically created flail leaflets inducing chronic mitral regurgitation were studied with two-dimensional (2D) echocardiography. Color Doppler M-mode images along the centerline of the accelerating flow towards the mitral regurgitation orifice were obtained. The distance between the two first aliasing boundaries (interaliasing distance [IAD]) was measured and the FC radius was mathematically derived according to the continuity equation (R(calc) = IAD/(1 - radicalv(1)/v(2)), v(1) and v(2) being the aliasing velocities). The conventional 2D FC radius was also measured (R(meas)). Mitral regurgitant volume was then calculated according to the FC method using both R(calc) and R(meas). Aortic and mitral electromagnetic (EM) flow probes and meters were balanced against each other to determine the reference standard MRV. RESULTS: Mitral regurgitant volume calculated from R(calc) and R(meas) correlated well with EM-MRV (y = 0.83x + 5.17, r = 0.90 and y = 1.04x + 0.91, r = 0.91, respectively, p < 0.001 for both). However, both methods resulted in slight overestimation of EM-MRV (Delta was 3.3 +/- 2.1 ml for R(calc) and 1.3 +/- 2.3 ml for R(meas)). CONCLUSIONS: Good correlation was observed between MRV derived from R(calc) (IAD method) and EM-MRV, similar to that observed with R(meas) (conventional FC method) and EM-MRV. The R(calc) using the IAD method has an advantage over conventional R(meas) in that it does not require spatial localization of the regurgitant orifice and can be performed semiautomatedly.

Relationship between early diastolic intraventricular pressure gradients, an index of elastic recoil, and improvements in systolic and diastolic function.

BACKGROUND: Early diastolic intraventricular pressure gradients (IVPGs) have been proposed to relate to left ventricular (LV) elastic recoil and early ventricular "suction." Animal studies have demonstrated relationships between IVPGs and systolic and diastolic indices during acute ischemia. However, data on the effects of improvements in LV function in humans and the relationship to IVPGs are lacking. METHODS AND RESULTS: Eight patients undergoing CABG and/or infarct exclusion surgery had a triple-sensor high-fidelity catheter placed across the mitral valve intraoperatively for simultaneous recording of left atrial (LA), basal LV, and apical LV pressures. Hemodynamic data obtained before bypass were compared with those with similar LA pressures and heart rates obtained after bypass. From each LV waveform, the time constant of LV relaxation (tau), +dP/dt(max), and -dP/dt(max) were determined. Transesophageal echocardiography was used to determined end-diastolic (EDV) and end-systolic (ESV) volumes and ejection fractions (EF). At similar LA pressures and heart rates, IVPG increased after bypass (before bypass 1.64+/-0.79 mm Hg; after bypass 2.67+/-1.25 mm Hg; P<0.01). Significant improvements were observed in ESV, as well as in apical and basal +dP/dt(max), -dP/dt(max), and tau (each P<0.05). Overall, IVPGs correlated inversely with both ESV (IVPG=-0.027[ESV]+3.46, r=-0.64) and EDV (IVPG=-0.027[EDV]+4.30, r=-0.70). Improvements in IVPGs correlated with improvements in apical tau (Deltatau =5.93[DeltaIVPG]+4.76, r=0.91) and basal tau (Deltatau =2.41[DeltaIVPG]+5.13, r=-0.67). Relative changes in IVPGs correlated with changes in ESV (DeltaESV=-0.97[%DeltaIVPG]+23.34, r=-0.79), EDV (DeltaEDV=-1.16[%DeltaIVPG]+34.92, r=-0.84), and EF (DeltaEF=0.38[%DeltaIVPG]-8.39, r=0.85). CONCLUSIONS: Improvements in LV function also increase IVPGs. These changes in IVPGs, suggestive of increases in LV suction and elastic recoil, correlate directly with improvements in LV relaxation and ESV.

Calculation of mitral regurgitant orifice area with use of a simplified proximal convergence method: initial clinical application.

To validate a previously proposed simplified proximal flow convergence method for calculating mitral regurgitant orifice area (ROA), a prospective study was conducted in ambulatory patients and in patients undergoing open heart surgery. Assuming a pressure difference between the left ventricle and left atrium of approximately 100 mm Hg (jet velocity [v(p)] 500 cm/s) and setting the color aliasing velocity (v(a)) to 40 cm/s, we simplified the conventional proximal convergence method formula (ROA = 2pi(r2)v(a)/v(p)) to r2/2, where r is the radius of the proximal convergence isovelocity hemisphere. For 57 ambulatory patients with a wide range of mitral regurgitant severity (1 to 4+), ROA was calculated by the conventional (x) and simplified (y) methods, demonstrating excellent accuracy (r = 0.92; P <.001; DeltaROA [y - x] = 0.004 +/- 0.08 cm2). For 24 intraoperative patients, ROA calculated by the simplified formula (y) correlated well with the pulsed Doppler-thermodilution method (x) (r = 0.84; P <.01; DeltaROA [y - x] = -0.002 +/- 0.08cm2). This simplified proximal convergence formula yields an accurate assessment of ROA for a wide range of regurgitant severity, while the time required for this measurement is shortened by half (1.5 +/- 0.5 minutes versus 3.2 +/- 0.7 minutes). This may increase the frequency of calculating ROA in the clinical laboratory.

Effect of cardiac output on mitral valve area in patients with mitral stenosis: validation and pitfalls of the pressure half-time method.

BACKGROUND AND AIM OF THE STUDY: The non-invasive evaluation of mitral valve area is often used in the assessment of patients with mitral stenosis. The pressure half-time method is commonly used to calculate valve area, but is inaccurate in many clinical scenarios. We sought to quantify the effects of changing cardiac output on the accuracy of mitral valve area determination. METHODS: Thirteen patients with mitral stenosis underwent routine stress echocardiography with resting and peak exercise results compared. A previously described and clinically validated mathematical model of the cardiovascular system was used to validate the clinical results. Seven different loading conditions for each of four different stenotic valve areas were modeled. RESULTS: In patients, with increasing cardiac output, pressure half-time decreased (-30.6+/-35.3 ms/l/min) and calculated valve area increased by 0.25+/-0.30 cm2/l/min. By continuity, it appeared that approximately half of this increase was due to actual valve orifice stretching, the remainder reflecting fundamental changes in the relationship between half-time and valve area. Mathematical modeling resulted in similar changes in pressure half-time and calculated valve area (0.06 to 0.12 cm2/l/min, p = 0.20 versus clinical results). CONCLUSION: Changes in cardiac output result in predictable changes in pressure half-time, and should be considered when performing serial examinations in patients with mitral stenosis.

Impact of tissue harmonic imaging on the assessment of rheumatic mitral stenosis.

We examined the effect of tissue harmonic imaging on the echocardiographic splitability score and valve area measurement of 40 patients with rheumatic mitral stenosis. Planimetered valve areas were unaffected by the use of harmonic imaging, but valve scores were increased, particularly in patients with scores <10.

Doppler echo evaluation of pulmonary venous-left atrial pressure gradients: human and numerical model studies.

The simplified Bernoulli equation relates fluid convective energy derived from flow velocities to a pressure gradient and is commonly used in clinical echocardiography to determine pressure differences across stenotic orifices. Its application to pulmonary venous flow has not been described in humans. Twelve patients undergoing cardiac surgery had simultaneous high-fidelity pulmonary venous and left atrial pressure measurements and pulmonary venous pulsed Doppler echocardiography performed. Convective gradients for the systolic (S), diastolic (D), and atrial reversal (AR) phases of pulmonary venous flow were determined using the simplified Bernoulli equation and correlated with measured actual pressure differences. A linear relationship was observed between the convective (y) and actual (x) pressure differences for the S (y = 0.23x + 0.0074, r = 0.82) and D (y = 0.22x + 0.092, r = 0.81) waves, but not for the AR wave (y = 0. 030x + 0.13, r = 0.10). Numerical modeling resulted in similar slopes for the S (y = 0.200x - 0.127, r = 0.97), D (y = 0.247x - 0. 354, r = 0.99), and AR (y = 0.087x - 0.083, r = 0.96) waves. Consistent with numerical modeling, the convective term strongly correlates with but significantly underestimates actual gradient because of large inertial forces.

Transient improvement of acetylcholine responses after short-term oral L-arginine in forearms of human heart failure.

Patients with heart failure exhibit impaired endothelium-dependent vasodilation. Although brief intraarterial administration of L-arginine improves endothelium-dependent vasodilatation in these patients, long-term oral supplementation is ineffective. To resolve these conflicting findings, we examined the effect of a single, short-term oral dose of L-arginine on serial, hourly forearm vascular responses to acetylcholine, sodium nitroprusside, and norepinephrine. Eighteen patients with heart failure were randomly allocated in a double-blinded, crossover study to receive either a single 20-g oral dose of L-arginine or placebo. Vascular responses were measured by forearm venous occlusion plethysmography before and at 60, 120, and 180 min after dosage. Blood was obtained for measurement of L-arginine and nitric oxide metabolite levels. Oral L-arginine increased plasma levels by fourfold at 60, 120, and 180 min. Vasodilatation to acetylcholine, 37 microg/min, was significantly enhanced at 60 min (percentage increase in forearm blood flow: placebo, 413 +/- 64%; L-arginine, 587 +/- 94%; p < 0.05), discernible at 120 min (p = 0.058) but no longer apparent at 180 min. Neither basal forearm blood flow, sodium nitroprusside, nor norepinephrine responses nor plasma levels of nitrite and nitrate were altered. We conclude that although short-term oral supplementation with L-arginine produced marked sustained elevation of plasma levels of L-arginine in patients with heart failure, responses to acetylcholine were only transiently improved.

Efficacy of anticoagulation in resolving left atrial and left atrial appendage thrombi: A transesophageal echocardiographic study.

BACKGROUND: Transesophageal echocardiography (TEE) is the gold standard for evaluation of the left atrium and the left atrial appendage (LAA) for the presence of thrombi. Anticoagulation is conventionally used for patients with atrial fibrillation to prevent embolization of atrial thrombi. The mechanism of benefit and effectiveness of thrombi resolution with anticoagulation is not well defined. METHODS AND RESULTS: We used a TEE database of 9058 consecutive studies performed between January 1996 and November 1998 to identify all patients with thrombi reported in the left atrium and/or LAA. One hundred seventy-four patients with thrombi in the left atrial cavity (LAC) and LAA were identified (1.9% of transesophageal studies performed). The incidence of LAA thrombi was 6.6 times higher than LAC thrombi (151 vs 23, respectively). Almost all LAC thrombi were visualized on transthoracic echocardiography (90.5%). Mitral valve pathology was associated with LAC location of thrombi (P <.0001), whereas atrial fibrillation or flutter was present in most patients with LAA location of thrombi. Anticoagulation of 47 +/- 18 days was associated with thrombus resolution in 80.1% of the patients on follow-up TEE. Further anticoagulation resulted in limited additional benefit. CONCLUSIONS: LAC thrombi are rare and are usually associated with mitral valve pathology. Transthoracic echocardiography is effective in identifying these thrombi. LAA thrombi occur predominantly in patients with atrial fibrillation or flutter. Short-term anticoagulation achieves a high rate of resolution of LAA and LAC thrombi but does not obviate the need for follow-up TEE.

Disk embolization of a Björk-Shiley convexo-concave mitral valve: a cause of sudden cardiovascular collapse and mesenteric ischemia.

Strut fracture and disk embolization of a Björk-Shiley convexo-concave valve is uncommon, but it should always be considered as a cause of sudden cardiovascular collapse in patients with such valves. Recognition of this clinical scenario is essential, given the importance of early diagnosis and the prevalence of these valves worldwide. We present a fatal case of disk embolization of a mitral prosthesis presenting with cardiogenic shock and mesenteric ischemia.