Decrease in longitudinal strain in heart transplant recipients is associated with rejection.

BACKGROUND: Around 20-40% of heart transplant patients experience moderate to severe rejection within the first year after heart transplantation. Endomyocardial biopsy (EMB) is a gold standard for diagnosing heart transplant rejection. There is a need for non-invasive alternatives that allow for early, safe and reliable diagnosis of acute graft rejection prior to the onset of clinical symptoms. AIMS: Our aim was to investigate the potential of speckle tracking derived strain analysis in the diagnosis of acute graft rejection. METHODS: Patients indicated for EMB consented to a trans-thoracic echocardiography examination (TTE) within 2 hours of the EMB. Of this cohort, those with at least 2 EMBs separated ≥ 1 week, and whose TTE could be analyzed for strain, were included. The relationship between strain and EMB results was evaluated. RESULTS: Of the 43 patients included (mean age 51.33±1.79, 67% male), 23 had findings of rejection identified on at least one EMB and at least one EMB without rejection for comparison. A significant deterioration in the longitudinal strain during rejection compared to non-rejection was found on apical 4-chamber views (-11.51±0.91 vs -13.48±0.96, P=0.025) and apical 2-chamber views (-11.84±0.78 vs -14.43±0.83, P=0.002). In the patients in whom no rejection was identified on either EBM, there was no significant change in longitudinal strain values at two different time points. CONCLUSION: Worsening of longitudinal strain was associated with acute cellular rejection. Routine TTE-based strain analysis could help in early detection of cardiac rejection and timing of EMB.

CD-NP: a novel engineered dual guanylyl cyclase activator with anti-fibrotic actions in the heart.

Natriuretic peptides (NPs) are cardioprotective through the activation of guanylyl cyclase (GC) receptors A and B. CD-NP, also known as cenderitide, is a novel engineered NP that was designed to uniquely serve as a first-in-class dual GC receptor agonist. Recognizing the aldosterone suppressing actions of GC-A activation and the potent inhibitory actions on collagen synthesis and fibroblast proliferation through GC-B activation, the current study was designed to establish the anti-fibrotic actions of CD-NP, administered subcutaneously, in an experimental rat model of early cardiac fibrosis induced by unilateral nephrectomy (UNX). Our results demonstrate that a two week subcutaneous infusion of CD-NP significantly suppresses left ventricular fibrosis and circulating aldosterone, while preserving both systolic and diastolic function, in UNX rats compared to vehicle treated UNX rats. Additionally we also confirmed, in vitro, that CD-NP significantly generates the second messenger, cGMP, through both the GC-A and GC-B receptors. Taken together, this novel dual GC receptor activator may represent an innovative anti-fibrotic therapeutic agent.

Concomitant use of beta-1 adrenoreceptor blocker and norepinephrine in patients with septic shock.

BACKGROUND: Betablockade has been shown to have cardioprotective effects in patients under perioperative stress. Besides animal model of septic shock and a small cohort of septic patients, these benefits have not been studied in septic shock patients who require norepinephrine administration. METHODS: After correction of preload, an esmolol bolus (0.2-0.5 mg/kg) followed by continuous 24 h infusion was administered in septic patients with sinus or supraventricular tachycardia (HR > 120/min). Exclusion criteria were severe LV systolic dysfunction, atrioventricular blockade and norepinephrine infusion at rates over 0.5 mg/kg/min. Monitoring with echocardiography and pulmonary artery catheter before, at 2, 6, 12, 24 h following the start and 6 h after ceasing of the esmolol drip. Patients were maintained normovolemic throughout the study and adjustments of concomitant norepinephrine infusion rates were made as required. RESULTS: Ten septic patients (mean age 54.4 ± 18.7), APACHE II 21.5 ± 6.2, CRP 275 ± 78 mg/l, procalcitonin 14.5 ± 10.1 mg/l, were given esmolol drip of 212.5 ± 63.5 mg/h at start to 272.5 ± 89.5 mg/h at 24 h. Heart rate decreased from mean 142 ± 11/min to 112 ± 9/min (p < 0.001) with parallel insignificant reduction of cardiac index (4.94 ± 0.76 to 4.35 ± 0.72 l/min/m(2)). Stroke volume insignificantly increased from 67.1 ± 16.3 ml to 72.9 ± 15.3 ml. No parallel change of pulmonary artery wedge pressure was observed (15.9 ± 3.2 to 15.0 ± 2.4 mmHg) as well as no significant changes of norepinephrine infusion (0.13 ± 0.17 to 0.17 ± 0.19 mg/kg/min), DO(2), VO(2), OER or arterial lactate. CONCLUSIONS: Saving the heart 30 beats/min did not demonstrate adverse impact on global haemodynamics in rates above 110/min. Using well titratable betablocker seems to be safe and cardioprotective in septic shock patients with high cardiac output.

Variable phenotype in murine transverse aortic constriction.

BACKGROUND: In mice, transverse aortic constriction (TAC) is variably characterized as a model of pressure overload-induced hypertrophy (left ventricular [LV] hypertrophy, or LVH) or heart failure (HF). While commonly used, variability in the TAC model is poorly defined. The objectives of this study were to characterize the variability in the TAC model and to define a simple, noninvasive method of prospectively identifying mice with HF versus compensated LVH after TAC. METHODS: Eight-week-old male C57BL/6J mice underwent TAC or sham and then echocardiography at 3 weeks post-TAC. A group of sham and TAC mice were euthanized after the 3-week echocardiogram, while the remainder underwent repeat echocardiography and were euthanized at 9 weeks post-TAC. The presence of TAC was assessed with two-dimensional echocardiography, anatomic aortic m-mode and color flow, and pulsed-wave Doppler examination of the transverse aorta (TA) and by LV systolic pressure (LVP). Trans-TAC pressure gradient was assessed invasively in a subset of mice. HF was defined as lung/body weight>upper limit in sham-operated mice. RESULTS: As compared with sham, TAC mice had higher TA velocity, LVP and LV weight, and lower ejection fraction (EF) at 3 or 9 weeks post-TAC. Only a subset of TAC mice (28%) developed HF. As compared with compensated LVH, HF mice were characterized by similar TA velocity and higher percent TA stenosis, but lower LVP, higher LV weight, larger LV cavity, lower EF and stress-corrected midwall fiber shortening, and more fibrosis. Both EF and LV mass measured by echocardiography at 3 weeks post-TAC were predictive of the presence of HF at 3 or 9 weeks post-TAC. CONCLUSIONS: In wild-type mice, TAC produces a variable cardiac phenotype. Marked abnormalities in LV mass and EF at echocardiography 3 weeks post-TAC identify mice with HF at autopsy. These data are relevant to appropriate design and interpretation of murine studies.

Experimental mild renal insufficiency mediates early cardiac apoptosis, fibrosis, and diastolic dysfunction: a kidney-heart connection.

Impaired renal function with loss of nephron number in chronic renal disease (CKD) is associated with increased cardiovascular morbidity and mortality. However, the structural and functional cardiac response to early and mild reduction in renal mass is poorly defined. We hypothesized that mild renal impairment produced by unilateral nephrectomy (UNX) would result in early cardiac fibrosis and impaired diastolic function, which would progress to a more global left ventricular (LV) dysfunction. Cardiorenal function and structure were assessed in rats at 4 and 16 wk following UNX or sham operation (Sham); (n = 10 per group). At 4 wk, blood pressure (BP), aldosterone, glomerular filtration rate (GFR), proteinuria, and plasma B-type natriuretic peptide (BNP) were not altered by UNX, representing a model of mild early CKD. However, UNX was associated with significantly greater LV myocardial fibrosis compared with Sham. Importantly, terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining revealed increased apoptosis in the LV myocardium. Further, diastolic dysfunction, assessed by strain echocardiography, but with preserved LVEF, was observed. Changes in genes related to the TGF-ß and apoptosis pathways in the LV myocardium were also observed. At 16 wk post-UNX, we observed persistent LV fibrosis and impairment in LV diastolic function. In addition, LV mass significantly increased, as did LVEDd, while there was a reduction in LVEF. Aldosterone, BNP, and proteinuria were increased, while GFR was decreased. The myocardial, structural, and functional alterations were associated with persistent changes in the TGF-ß pathway and even more widespread changes in the LV apoptotic pathway. These studies demonstrate that mild renal insufficiency in the rat results in early cardiac fibrosis and impaired diastolic function, which progresses to more global LV remodeling and dysfunction. Thus, these studies importantly advance the concept of a kidney-heart connection in the control of myocardial structure and function.

Standard blood flow rates of cardiopulmonary bypass are adequate in awake on-pump cardiac surgery.

OBJECTIVE: Standard blood flow rates for cardiopulmonary bypass have been assumed to be the same for awake cardiac surgery with thoracic epidural anesthesia (TEA) as for general anesthesia. However, compared with general anesthesia, awake cardiac surgery with epidural anesthesia may be associated with higher oxygen consumption and may result in lactic acidosis when standard blood flow rates were used. The aim of our study was to investigate if standard blood flow rates are adequate in awake cardiac surgery. METHODS: Forty-five patients undergoing elective on-pump cardiac surgery were assigned to receive either epidural (Group TEA, n=15), combined (Group TEA-GA, n=15) or general (Group GA, n=15) anesthesia. To monitor the adequacy of standard blood flow rates, arterial lactate, acid base parameters, and central venous and jugular bulb saturation were measured at six time points (before, during, and after the surgery) in all groups. Blood flow rates were adjusted when needed. RESULTS: No lactic acidosis has developed in any group (p=NS). TEA as compared with TEA-GA and GA groups had lower central venous (67±4%, 75±11%, and 72±13%, respectively, p<0.05) and jugular bulb oxygen saturations during cardiopulmonary bypass (60±7%, 68±9%, and 75±12%, respectively, p<0.05) during the post-cardiopulmonary bypass period. The TEA group as compared with the TEA-GA and GA groups also had mild hypercapnic respiratory acidosis (56±10, 42±8, and 37±4 mmHg, respectively, p<0.05) and mild decrease of arterial oxygen saturation (93±4%, 97±2%, and 96±1%, respectively, p<0.05) at the end of surgery without any clinical consequences. Thus, no additional blood flow rates adjustments in any study group and no ventilatory support in TEA group were required. CONCLUSIONS: Under careful monitoring, the use of standard blood flow rates is adequate for patients undergoing awake on-pump normothermic cardiac surgery.

Estimation of left ventricular filling pressures by speckle tracking echocardiography in patients with idiopathic dilated cardiomyopathy.

AIMS: the ratio of early diastolic transmitral flow velocity (E) to early diastolic mitral annular velocity (E(a)) is frequently used to predict an increase in left ventricular filling pressure (LVFP). However, this approach has several limitations. The aim of this study was to test whether additional information is gained by new echocardiographic indexes utilizing strain and strain rate (SR) derived from 2-dimensional speckle tracking echocardiography (2D-STE) for the estimation of LVFP. METHODS AND RESULTS: fifty-one patients with idiopathic dilated cardiomyopathy (IDC) underwent pulsed-wave tissue Doppler echocardiography and 2D-STE performed simultaneously with right heart catheterization. Receiver operating characteristic analysis showed that circumferential strain and the SR during late diastolic LV filling (0.956 and 0.951, both P = 0.001), E/circumferential SR at early diastolic LV filling (0.949, P = 0.001), and E/circumferential strain at the time of peak E-wave (0.948, P = 0.001) had greater area under the curve than the E/E(a) ratio (0.911, P = 0.001) for the prediction of pulmonary capillary wedge pressure > 12 mmHg. CONCLUSION: when compared with the E/E(a) ratio, several 2D-STE-derived parameters better estimated the increase in LVFP in patients with IDC.

Mineralocorticoid accelerates transition to heart failure with preserved ejection fraction via "nongenomic effects".

BACKGROUND: Mechanisms promoting the transition from hypertensive heart disease to heart failure with preserved ejection fraction are poorly understood. When inappropriate for salt status, mineralocorticoid (deoxycorticosterone acetate) excess causes hypertrophy, fibrosis, and diastolic dysfunction. Because cardiac mineralocorticoid receptors are protected from mineralocorticoid binding by the absence of 11-beta hydroxysteroid dehydrogenase, salt-mineralocorticoid-induced inflammation is postulated to cause oxidative stress and to mediate cardiac effects. Although previous studies have focused on salt/nephrectomy in accelerating mineralocorticoid-induced cardiac effects, we hypothesized that hypertensive heart disease is associated with oxidative stress and sensitizes the heart to mineralocorticoid, accelerating hypertrophy, fibrosis, and diastolic dysfunction. METHODS AND RESULTS: Cardiac structure and function, oxidative stress, and mineralocorticoid receptor-dependent gene transcription were measured in sham-operated and transverse aortic constriction (studied 2 weeks later) mice without and with deoxycorticosterone acetate administration, all in the setting of normal-salt diet. Compared with sham mice, sham plus deoxycorticosterone acetate mice had mild hypertrophy without fibrosis or diastolic dysfunction. Transverse aortic constriction mice displayed compensated hypertensive heart disease with hypertrophy, increased oxidative stress (osteopontin and NOX4 gene expression), and normal systolic function, filling pressures, and diastolic stiffness. Compared with transverse aortic constriction mice, transverse aortic constriction plus deoxycorticosterone acetate mice had similar left ventricular systolic pressure and fractional shortening but more hypertrophy, fibrosis, and diastolic dysfunction with increased lung weights, consistent with heart failure with preserved ejection fraction. There was progressive activation of markers of oxidative stress across the groups but no evidence of classic mineralocorticoid receptor-dependent gene transcription. CONCLUSIONS: Pressure-overload hypertrophy sensitizes the heart to mineralocorticoid excess, which promotes the transition to heart failure with preserved ejection fraction independently of classic mineralocorticoid receptor-dependent gene transcription.

Regulation of circulating progenitor cells in left ventricular dysfunction.

BACKGROUND: Reductions in numbers of circulating progenitor cells (CD34+ cell subsets) have been demonstrated in patients at risk for, or in the presence of, cardiovascular disease. The mediators of these reductions remain undefined. To determine whether neurohumoral factors might regulate circulating CD34+ cell subsets in vivo, we studied complementary canine models of left ventricular (LV) dysfunction. METHODS AND RESULTS: A pacing model of severe LV dysfunction and a hypertensive renal wrap model in which dogs were randomized to receive deoxycorticosterone acetate (DOCA) were studied. Circulating CD34+ cell subsets including hematopoietic precursor cells (HPCs: CD34+/CD45(dim)/VEGFR2-) and endothelial progenitor cells (EPCs: CD34+/CD45-/VEGFR2+) were quantified. Additionally, the effect of mineralocorticoid excess on circulating progenitor cells in normal dogs was studied. The majority of circulating CD34+ cells expressed CD45dimly and did not express VEGFR2, consistent with an HPC phenotype. HPCs were decreased in response to pacing, and this decrease correlated with plasma aldosterone levels (Spearman rank correlation=-0.67, P=0.03). In the hypertensive renal wrap model, administration of DOCA resulted in decreased HPCs. No changes were seen in EPCs in either model. Normal dogs treated with DOCA exhibited a decrease in HPCs in peripheral blood but not bone marrow associated with decreased telomerase activity. CONCLUSIONS: This is the first study to demonstrate that mineralocorticoid excess, either endogenous or exogenous, results in reduction in HPCs. These data suggest that mineralocorticoids may induce accelerated senescence of progenitor cells, leading to their reduced survival and decline in numbers.

Normal weight obesity: a risk factor for cardiometabolic dysregulation and cardiovascular mortality.

AIMS: We hypothesized that subjects with a normal body mass index (BMI), but high body fat (BF) content [normal weight obesity (NWO)], have a higher prevalence of cardiometabolic dysregulation and are at higher risk for cardiovascular (CV) mortality. METHODS AND RESULTS: We analysed 6171 subjects >20 years of age from the Third National Health and Nutrition Examination Survey (NHANES III) and the NHANES III mortality study, whose BMI was within the normal range (18.5-24.9 kg/m(2)), and who underwent a complete evaluation that included body composition assessment, blood measurements, and assessment of CV risk factors. Survival information was available for >99% of the subjects after a median follow-up of 8.8 years. We divided our sample using sex-specific tertiles of BF%. The highest tertile of BF (>23.1% in men and >33.3% in women) was labelled as NWO. When compared with the low BF group, the prevalence of metabolic syndrome in subjects with NWO was four-fold higher (16.6 vs. 4.8%, P < 0.0001). Subjects with NWO also had higher prevalence of dyslipidaemia, hypertension (men), and CV disease (women). After adjustment, women with NWO showed a significant 2.2-fold increased risk for CV mortality (HR = 2.2; 95% CI, 1.03-4.67) in comparison to the low BF group. CONCLUSION: Normal weight obesity, defined as the combination of normal BMI and high BF content, is associated with a high prevalence of cardiometabolic dysregulation, metabolic syndrome, and CV risk factors. In women, NWO is independently associated with increased risk for CV mortality.

Left ventricular mechanics in idiopathic dilated cardiomyopathy: systolic-diastolic coupling and torsion.

BACKGROUND: In idiopathic dilated cardiomyopathy (IDC), myocardial deformational parameters and their mutual relationships remain incompletely characterized. METHODS: Thirty-seven patients with IDC underwent two-dimensional speckle-tracking echocardiography (2D-STE) to assess left ventricular rotation, torsion, and longitudinal, circumferential, and radial systolic and diastolic strains and strain rates. Additionally, 2D-STE was performed in 14 controls. RESULTS: All deformational parameters on 2D-STE were significantly lower in patients with IDC compared with controls. Seven patients exhibited opposite basal (positive, counterclockwise) and 11 patients exhibited opposite apical (negative, clockwise) rotation at end-systole. Circumferential, radial, and longitudinal early diastolic strain rates were correlated most strongly with the corresponding spatial components of systolic deformation. CONCLUSION: In patients IDC, all torsional, systolic, and diastolic deformational parameters were decreased. Corresponding three-dimensional components of systolic and diastolic deformations were closely coupled. Considerable variation in the direction of basal and apical rotation exists in a subset of patients with IDC.

Dynamic changes of left ventricular performance and left atrial volume induced by the mueller maneuver in healthy young adults and implications for obstructive sleep apnea, atrial fibrillation, and heart failure.

Using the Mueller maneuver (MM) to simulate obstructive sleep apnea (OSA), our aim was to investigate acute changes in left-sided cardiac morphologic characteristics and function which might develop with apneas occurring during sleep. Strong evidence supports a relation between OSA and both atrial fibrillation and heart failure. However, acute effects of airway obstruction on cardiac structure and function have not been well defined. In addition, it is unclear how OSA might contribute to the development of atrial fibrillation and heart failure. Echocardiography was used in healthy young adults to measure various parameters of cardiac structure and function. Subjects were studied at baseline, during, and immediately after performance of the MM and after a 10-minute recovery. Continuous heart rate, blood pressure, and pulse oximetry measurements were made. During the MM, left atrial (LA) volume index markedly decreased. Left ventricular (LV) end-systolic dimension increased in association with a decrease in LV ejection fraction. On release of the maneuver, there was a compensatory increase in blood flow to the left side of the heart, with stroke volume, ejection fraction, and cardiac output exceeding baseline. After 10 minutes of recovery, all parameters returned to baseline. In conclusion, sudden imposition of severe negative intrathoracic pressure led to an abrupt decrease in LA volume and a decrease in LV systolic performance. These changes reflected an increase in LV afterload. Repeated swings in afterload burden and chamber volumes may have implications for the future development of atrial fibrillation and heart failure.

Nesiritide in acute decompensated heart failure: current status and future perspectives.

Acute decompensated heart failure (ADHF) is a growing public health problem with high mortality and costs. ADHF often, if not usually, occurs in the setting of cardiovascular and noncardiovascular comorbidities as well as advanced age. New insights provide support for the concept of heart failure as a state of deficiency of and/or resistance to endogenous B-type natriuretic peptide. The primary goals of ADHF therapy are to relieve symptoms and optimize volume status with minimal side effects. Few therapies are proven to effectively do so. Nesiritide is a balanced vasodilator with favorable neurohumoral effects and is superior to placebo in providing rapid symptom relief and to nitroglycerin in reducing filling pressures. Recent trials confirm a lack of renal toxicity at recommended doses. An adequately powered multinational mortality trial is underway. Nesiritide represents a proven therapy for normotensive/hypertensive ADHF patients with severe symptoms at rest.

Insights into natriuretic peptides in heart failure: an update.

Natriuretic peptides (NPs) secreted by the heart in response to volume overload are pleiotropic molecules with vasodilating, diuretic, natriuretic, antiproliferative, and antifibrotic actions. Functioning of the NP system is altered in congestive heart failure (CHF), suggesting that support of the NP system might be beneficial in treatment of acute and chronic CHF. Several approaches alone or in combination with other pharmacologic therapies have been shown to enhance function of the NP system: direct administration of native and designer NPs, inhibition of degradation of NPs and their second messenger (cyclic guanosine monophosphate ), and stimulation of cGMP generation. Despite increasing numbers of studies using NPs in therapy of acute and chronic CHF, several controversies regarding safety, efficacy, and dosing of NPs need to be addressed. Moreover, further research is warranted to identify the stages and etiologies of CHF that may profit from NP therapy.

Comparison of usefulness of tissue Doppler imaging versus brain natriuretic peptide for differentiation of constrictive pericardial disease from restrictive cardiomyopathy.

Brain (B-type) natriuretic peptide (BNP) and tissue Doppler imaging may distinguish restrictive cardiomyopathy (RCMP) from idiopathic constrictive pericardial disease (CP). However, their comparative efficacy is unknown for patients with CP from secondary causes (e.g., surgery or radiotherapy). We compared the efficacy of tissue Doppler imaging and BNP for differentiation of RCMP (n = 15) and CP (n = 16) were compared. BNP was higher in patients with RCMP than CP (p = 0.008), but the groups overlapped, particularly for BNP <400 pg/ml. BNP was lower with idiopathic CP than secondary CP (139 +/- 50 vs 293 +/- 69 pg/ml; p <0.001) or RCMP (139 +/- 50 vs 595 +/- 499 pg/ml; p <0.001), but not significantly different between those with secondary CP and RCMP (293 +/- 69 vs 595 +/- 499 pg/ml; p = 0.1). Patients with CP and RCMP had less overlap in early diastolic and isovolumic contraction tissue Doppler imaging velocities compared with BNP, with clear separation of groups evident with mean early diastolic annular velocities (averaged from 4 walls). Early diastolic tissue Doppler imaging velocity was superior to BNP for differentiation of CP and RCMP (area under the curve 0.97 vs 0.76, respectively; p = 0.01). In conclusion, mean early diastolic mitral annular velocity correctly distinguished CP from RCMP even when there was a large overlap of BNP between the 2 groups.

Relationships between leptin and C-reactive protein with cardiovascular disease in the adult general population.

BACKGROUND: Leptin could be a key regulator of C-reactive protein (CRP) levels, which serve as a marker of systemic inflammation. Both leptin and CRP are predictors of cardiovascular disease (CVD). However, the interactions between leptin and CRP, and their association with CVD, remain unclear. We therefore studied them in a large, multiethnic population. METHODS: We analyzed leptin and CRP levels, anthropometric variables and cardiovascular risk factor data from 6,251 participants from the Third National Health and Nutrition Examination Survey (NHANES III). Logistic regression was used to estimate the association between leptin, CRP and CVD (defined as history of myocardial infarction or stroke). Receiver operating characteristic curves were created to study the additional value of leptin and CRP for the association with CVD. RESULTS: The mean age was 44.4 +/- 0.21 years (52.5% women). After adjustment for age, race, dyslipidemia, hypertension, diabetes, smoking, obesity and CRP, high levels of leptin were significantly associated with CVD in men (odds ratio 2.47, 95% CI 1.19-5.19) and in women (odds ratio 3.30, 95% CI 1.47-7.99). After adjustment for leptin, CRP was not associated with CVD. There was a significant correlation between levels of leptin and CRP (Spearman correlation rho = 0.22 in men and rho = 0.32 in women, both P < 0.0001). The area under the curve, representing the association between cardiovascular risk factors and CVD, increased after the addition of high levels of both leptin and CRP together. CONCLUSION: High leptin levels are independently associated with CVD even after adjustment for CRP; elevated CRP levels are not associated with CVD after adjustment for leptin. However, increased concentrations of both leptin and CRP confer the highest risk for CVD.

Doppler strain imaging closely reflects myocardial energetic status in acute progressive ischemia and indicates energetic recovery after reperfusion.

BACKGROUND: Capitalizing on mechanoenergetic coupling, we investigated whether strain echocardiography can noninvasively estimate the ratio of adenosine triphosphate (ATP) to adenosine diphosphate (ADP), a marker of energetic status during acute myocardial ischemia and reperfusion. METHODS: Twenty-eight pigs were divided into 7 groups (1 baseline, 4 ischemic, and 2 reperfusion). Ischemia was induced by left anterior descending coronary artery occlusion. Longitudinal systolic lengthening (SL) and postsystolic shortening (PSS) strain were measured by echocardiography. The ATP/ADP ratio was obtained from myocardial biopsies in the ischemic and control regions. RESULTS: SL and PSS strain and the ATP/ADP ratio progressively decreased (P < .05) with increased duration (12, 40, 120, and 200 minutes) of ischemia. A mathematical formula (ATP/ADP = -0.97 + 0.25 x PSS strain + 0.20 x SL strain) estimated best the ATP/ADP ratio (r = 0.94, P < .05). Reperfusion after 12 but not after 120 minutes of ischemia significantly improved the ATP/ADP ratio and decreased SL and PSS strain. CONCLUSIONS: Strain echocardiography closely reflected changes and enabled the noninvasive estimation of the ATP/ADP ratio. A higher ATP/ADP ratio is associated with functional improvement after reperfusion.

Classification of acute myocardial ischemia by artificial neural network using echocardiographic strain waveforms.

Echocardiographic strain waveforms are highly variable, so their interpretation is experience-dependent and subjective. We tested whether an artificial neural network (ANN) can distinguish between strain waveforms obtained at baseline and during experimentally induced acute ischemia. An open-chest model of coronary occlusion and acute ischemia was used in 14 adult pigs. Strain waveforms were obtained using a GE Vivid 7 ultrasound system. An ANN design was implemented in MATLAB, and backpropagation and "leave-one-out" processes were used to train and test it. Specificity of 86% and sensitivity of 87% suggest that ANNs could aid in diagnostic prescreening of echocardiographic strain waveforms.

Hepatic tear as an elusive cause of hemoperitoneum complicating cardiac surgery.

We report an unusual source of intra-operative bleeding in a patient undergoing cardiosurgical reoperation. After sternotomy, hematocrit dropped significantly. Only intra-thoracic bleeding from adhesions was considered to be responsible for the anemia. During reperfusion, abdominal wall was distended with a bluish bulge in the right hemidiaphragm. Immediate laparotomy revealed bleeding from a tear in the right hepatic lobe without any diaphragm injury. The tear was likely caused by blunt trauma from an oscillating saw. We emphasize cautious use of an oscillating saw in patients with hepatic congestion undergoing a repeat sternotomy. We propose that lifting the sternum in redo procedures might prevent the hepatic tear.