Basal Segmental Longitudinal Strain: A Marker of Subclinical Myocardial Involvement in Anderson-Fabry Disease.

BACKGROUND: Cardiac involvement in Anderson-Fabry disease (AFD) is associated with increased left ventricular (LV) wall thickness. The aim of this study was to evaluate if two-dimensional global and regional strain in patients with AFD can identify early myocardial involvement (when LV wall thickness and function are normal). Additionally, the association of altered strain with adverse cardiovascular events was evaluated. METHODS: In a retrospective cross-sectional study, 43 patients with AFD, before enzyme replacement therapy (mean age, 44 ± 12 years; 58.1% men), were compared with age- and gender-matched healthy control subjects. The mean follow-up duration among patients with AFD for major adverse cardiovascular events (MACE) was 82 months. RESULTS: LV ejection fraction was similar between groups (patients with AFD vs control subjects, 61 ± 8% vs 61 ± 6%; P = .89). However, global longitudinal strain (LS) was impaired in patients with AFD compared with control subjects (-16.5 ± 3.8% vs -20.2 ± 1.7%, P < .001), with greater impairment in patients with AFD with increased LV wall thickness (-15.4 ± 3.9% vs -18.7 ± 2.3%, P < .006). Additionally, LS was most impaired in the basal segments in patients with AFD (-14.8 ± 3.7% vs -20.3 ± 1.1%, P < .001). MACE occurred in 19 of 43 patients (four women, 15 men), and Kaplan-Meier analysis demonstrated that MACE were associated with impaired basal LS. CONCLUSIONS: In patients with AFD, altered basal LS is present even in those with normal LV wall thickness and is associated with MACE. Therefore, basal LS should be considered when screening for cardiac involvement in AFD, particularly in female patients with AFD with normal LV wall thickness.

The impact of incomplete revascularization on early and late outcomes in ST-elevation myocardial infarction.

BACKGROUND: In ST-elevation myocardial infarction (STEMI) in patients with multivessel disease, there is a lack of consensus regarding the importance of complete revascularization and the timing of treatment of nonculprit stenoses. Our objective was to investigate the impact of incomplete revascularization in STEMI patients using the residual Synergy Between PCI with TAXUS and Cardiac Surgery score (rSS) to define completeness of revascularization. METHODS: This study examined associations between incomplete revascularization, determined by the rSS, and the combined outcome of cardiac death and myocardial infarction (MI). Patients were divided into groups: rSS = 0 (complete revascularization), rSS = 1-8 (incomplete revascularization with a low burden of residual disease), or rSS >8 (incomplete revascularization with a high burden of residual disease). RESULTS: The rSS score was calculated in 589 consecutive patients; 25% had an rSS of 0, 42% rSS 1-8, and 33% rSS >8. At median follow-up of 3.5 years, cardiac death and MI occurred in 5% of rSS = 0 patients, 15% rSS = 1-8, and 26% with rSS >8 (P < .001). The rSS was powerful independent predictor of cardiac death and MI (hazard ratio 5.05, CI 2.89-12.00, rSS >8 vs rSS 0, P < .001 and hazard ratio 2.96, CI 1.31-6.69, rSS = 1-8 vs rSS = 0, P = .009), respectively, and an independent predictor of mortality, MI, unplanned revascularization, and major adverse cardiovascular events. CONCLUSIONS: In patients with STEMI, the rSS independently predicts cardiac death and MI. Patients with an rSS >8 had substantially higher rates of cardiac death or MI. The rSS can be used to define incomplete revascularization in STEMI and predict adverse outcomes.

Electrocardiographic measurement of infarct size compared to cardiac MRI in reperfused first time ST-segment elevation myocardial infarction.

BACKGROUND: Myocardial infarct size (IS) following ST-segment elevation myocardial infarction (STEMI) is an important prognostic factor. We assessed the Selvester 32-point QRS score from the 12-lead ECG for measurement of IS in STEMI patients receiving reperfusion therapy compared to cardiac magnetic resonance imaging (CMRI). Furthermore we sought to explore the impact of microvascular obstruction (MVO) on the scoring system, and determine factors contributing to discrepancies between CMRI IS and Selvester score. METHODS: We examined 70 patients (55 men, 15 women), mean age 57±10years with a first time STEMI (46 anterior, 24 non-anterior). QRS scores were calculated early and at follow-up (mean 2±1 and 59±14days post-STEMI). Myocardial core scar size (5SD) was measured at 5.3±3.3 and 57.8±13.5days post-infarction by CMRI. MVO was determined on initial MRI. Logistic regression analysis was performed to determine factors contributing to discordant scores, defined as a difference between CMRI and Selvester IS of >6% myocardium. RESULTS: QRS scoring of anterior infarcts correlated with CMRI IS both early (r=0.734, p<0.0001) and at follow-up (r=0.716, p<0.0001); however no correlation was seen among non-anterior infarcts. QRS scoring overestimated IS at all time points. There was better agreement between ECG and CMRI measured IS in patients without MVO at both time points. Anterior infarction was inversely predictive of discordant IS estimation acutely, and larger Selvester scores were predictive of inaccurate scoring at both time periods. CONCLUSIONS: Selvester QRS score correlates well with CMRI IS for anterior infarcts. MVO did not independently affect the score.

Prognostic value of high sensitivity troponin T after ST-segment elevation myocardial infarction in the era of cardiac magnetic resonance imaging.

AIMS: To determine if high sensitivity troponin T (hs-TnT) measurements performed during the 'plateau phase' of troponin release (≥48 h) following ST-segment elevation myocardial infarction (STEMI) can predict major adverse cardiovascular endpoints (MACE), and to evaluate its prognostic value compared with cardiac magnetic resonance imaging (CMRI) parameters. METHODS AND RESULTS: We prospectively recruited 201 first presentation STEMI patients. Serial hs-TnT levels were measured at admission, peak (highest), 24, 48 and 72 h. CMRI and transthoracic echocardiography were performed (4 days median) post-STEMI, evaluating infarct scar characteristics and left ventricular ejection fraction (LVEF). Associations were determined between hs-TnT levels and CMRI parameters early after STEMI with MACE (comprising mortality, re-infarction, new or worsening of heart failure, cerebrovascular accident, and sustained ventricular arrhythmias) at medium-term follow-up. After 602 days (median), 33 (17%) patients had MACE. Upper tertile hs-TnT levels at 48 and 72 h were associated with MACE (Kaplan-Meier P = 0.002 and P = 0.012, respectively). Multivariate Cox analyses, incorporating diabetes, CMRI scar size, LVEF and hs-TnT levels (applied at a single hs-TnT time point) showed that 48 and 72 h hs-TnT levels were independent predictors for MACE (HR = 1.20, P = 0.002, and HR = 1.21, P = 0.035 respectively). CONCLUSION: Measurement of hs-TnT in the plateau phase after STEMI is an inexpensive method of prognostic risk assessment.

High-sensitivity troponin T predicts infarct scar characteristics and adverse left ventricular function by cardiac magnetic resonance imaging early after reperfused acute myocardial infarction.

BACKGROUND: Late gadolinium enhancement cardiac magnetic resonance imaging (CMRI) is the current standard for evaluation of myocardial infarct scar size and characteristics. Because post-ST-segment elevation myocardial infarction (STEMI) troponin levels correlate with clinical outcomes, we sought to determine the sampling period for high-sensitivity troponin T (hs-TnT) that would best predict CMRI-measured infarct scar characteristics and left ventricular (LV) function. METHODS AND RESULTS: Among 201 patients with first presentation with STEMI who were prospectively recruited, we measured serial hs-TnT levels at admission, peak, 24 hours, 48 hours, and 72 hours after STEMI. Indexed LV volumes, LV ejection fraction (LVEF) and infarct scar characteristics (scar size, scar heterogeneity, myocardial salvage index, and microvascular obstruction) were evaluated by CMRI at a median of 4 days post-STEMI. Peak and serial hs-TnT levels correlated positively with early indexed LV volumes and infarct scar characteristics, and negatively correlated with myocardial salvage index and LVEF. Both 48- and 72-hour hs-TnT levels similarly predicted "large" total infarct scar size (odds ratios [ORs] 3.08 and 3.53, both P < .001), myocardial salvage index (ORs 1.68 and 2.30, both P < .001), and LVEF <40% (ORs 2.16 and 2.17, both P < .001) on univariate analyses. On multivariate analyses, 48- and 72-hour hs-TnT levels independently predicted large infarct scar size (ORs 2.05 and 2.31, both P < .001), reduced myocardial salvage index (OR 1.39 [P = .031] and OR 1.55 [P = .009]), and LVEF <40% (OR 1.47 [P = .018] and OR 1.43 [P = .026]). All measured hs-TnT levels had a modest association and similar capacity to predict microvascular obstruction. CONCLUSIONS: Levels of hs-TnT at 48 and 72 hours, measured during the "plateau phase" post-STEMI, predicted infarct scar size, poor myocardial salvage, and LVEF. These levels also correlated with scar heterogeneity and microvascular obstruction post-STEMI. Since ascertaining peak levels after STEMI is challenging in routine practice, based on the biphasic kinetics of hs-TnT, a measurement at 48 to 72 hours (during the plateau phase) provides a useful and simple method for early evaluation of LV function and infarct scar characteristics.

Left atrial enlargement and reduced atrial compliance occurs early in Fabry cardiomyopathy.

BACKGROUND: Fabry disease is associated with left ventricular hypertrophy (LVH) and myocardial fibrosis. The aim of this study was to evaluate left atrial (LA) size and function using tissue Doppler-derived strain in patients with Fabry disease. METHODS: Echocardiography was performed in 33 Fabry patients (14 without LVH, 19 with LVH) before commencement of enzyme replacement therapy, and results were compared with those from age-matched and gender-matched controls (n=28 and n=38, respectively). Atrial strain and strain rate were measured from four segments in the apical four-chamber and two-chamber views of the LA, and global values were calculated. Systolic strain, systolic strain rate, early diastolic strain rate, and late diastolic strain rate were measured. Phasic LA volumes and fractions were calculated. Mitral inflow and tissue Doppler E' velocities were used to estimate left ventricular (LV) diastolic function. RESULTS: LA volume was increased in Fabry patients, even in the absence of LVH. Importantly, diastolic function was normal in this subgroup without LVH, with E' velocities similar to those in controls. LA systolic strain and early diastolic strain rate were selectively reduced in Fabry patients with LVH and reflect reductions in LA and LV relaxation, respectively, consequent to increased LV mass. However, independent of LVH, both Fabry groups had significant reductions in systolic strain rate and increased LA stiffness index. CONCLUSIONS: Fabry disease is associated with LA enlargement and reduced atrial compliance that occurs before the development of LVH. This suggests that Fabry cardiomyopathy may not only cause ventricular hypertrophy and fibrosis but also alters atrial myocardial properties early in the disease process. Consequently, measurements of LA size and function may be useful in the early diagnosis of Fabry disease, before the development of LVH.

Left ventricular systolic function in HER2/neu negative breast cancer patients treated with anthracycline chemotherapy: a comparative analysis of left ventricular ejection fraction and myocardial strain imaging over 12 months.

AIM: Anthracycline agents are undermined by their cardiotoxicity. As life expectancy following treatment is greatly improved, techniques that ensure early detection and timely management of cardiotoxicity are essential. The aim of the present study was to evaluate left ventricular (LV) systolic function with LV ejection fraction (LVEF) and two-dimensional myocardial strain up to 12 months after anthracycline chemotherapy, specifically in HER2/neu negative breast cancer patients. METHODS: Seventy-eight consecutive anthracycline naïve breast cancer patients were studied before and immediately after anthracycline chemotherapy. Fifty HER2/neu negative patients were studied over 12 months with serial echocardiograms at four time points. All patients were treated with standard regimens containing anthracyclines. RESULTS: Global systolic strain was significantly reduced immediately after, and 6 months after anthracyclines (-19.0 ± 2.3% to -17.5 ± 2.3% (P<0.001) and -18.2 ± 2.2% (P=0.01) respectively). A non-uniform reduction in strain was observed each time with relative sparing of the LV apex. LVEF remained largely unchanged at both time points. Global strain normalised by 12 months in the majority of patients. Persistently reduced strain was observed in 16% (n=8); these patients had a greater reduction in strain at 6 months (≤ -17.2%), and had received higher cumulative anthracycline doses. CONCLUSION: Myocardial strain imaging is more sensitive than LVEF for the early detection and intermediate term monitoring of LV systolic function following anthracycline chemotherapy in HER2/neu negative breast cancer patients, and may aid in the development of improved monitoring protocols.

Hypertension accelerates the 'normal' aging process with a premature increase in left atrial volume.

Hypertension (HT) is associated with left ventricular (LV) diastolic dysfunction and consequent left atrial (LA) dilatation. We investigated changes in LA size and phasic function by decade in patients with HT. Patients with mild or moderate HT (n = 122) were compared with a case controlled normal cohort (blood pressure <140/90 mm Hg). Biplane LA maximum, minimum, and pre 'a' wave volumes were measured; LA filling, passive emptying, and active emptying volumes and fractions were calculated. Transmitral inflow and pulsed wave mitral annular tissue Doppler velocity were measured as expressions of LV diastolic function. The HT group had larger LA maximum volumes compared with normal controls for all decades until the 8th decade. Subjects with HT in decade 4 had LA maximum volume similar to that of normal controls from decade 8 (27.8 ± 4.3 mL/m(2) vs 25.6 ± 6.1 mL/m(2) respectively, P = .22). Active emptying volume and fraction were higher in the HT group across all decades, while there was no difference between the HT and normal groups for passive emptying volume. LV mass and E/E' ratio were significantly higher across all decades in the HT group. HT alters atrial dynamics significantly, with resultant increased LA volume and active emptying volume consequent to altered LV diastolic function. HT 'accelerates' the normal aging process with patients as early as decade 4 having similar LA size to that of normal controls in decade 8. This premature increase in LA volume may result in the future development of atrial fibrillation in HT patients.

Altered left ventricular longitudinal diastolic function correlates with reduced systolic function immediately after anthracycline chemotherapy.

AIMS: The benefits from anthracycline chemotherapy are undermined by potentially life-threatening cardiotoxicity. Transthoracic echocardiography is the most commonly used method for monitoring cardiotoxicity, and centres on the measurement of left ventricular systolic function. The aim of this study was to utilize two-dimensional speckle tracking echocardiography (2DSTE) at baseline and immediately after anthracycline chemotherapy to investigate whether patients with significant changes in systolic function after anthracycline therapy would also develop alterations in diastolic parameters. METHODS AND RESULTS: Fifty-two women with histologically confirmed breast cancer were prospectively recruited. Echocardiograms were performed 1 week prior to and 1 week following chemotherapy (always before adjuvant trastuzumab or thoracic radiotherapy). Conventional Doppler, tissue velocity imaging (TVI), and 2DSTE were used to measure diastolic function. 2DSTE measurements included longitudinal diastolic strain, early (E-Sr), and late (A-Sr) myocardial strain rate. 2DSTE and left ventricular ejection fraction (LVEF) were used to measure longitudinal systolic function. Altered LV diastolic function (including E-Sr) was observed in the entire cohort after chemotherapy, with a differential reduction in participants with a post therapy LVEF <55%. Pre-chemotherapy systolic strain was found to predict reduced E-Sr post therapy (P = 0.04). Univariate predictors of E-Sr were LVEF post therapy (P = 0.049) and systolic strain post-therapy (P = 0.01). In a multivariate analysis, systolic strain after chemotherapy was the strongest independent predictor (P = 0.001). CONCLUSION: Altered LV diastolic function was observed immediately after the administration of therapeutic doses of anthracycline chemotherapy. Furthermore, our analysis indicates that the changes in diastolic function are associated with reduced systolic function.

Left ventricular mass predicts left atrial appendage thrombus in persistent atrial fibrillation.

AIMS: Atrial fibrillation (AF) can result in the development of left atrial appendage (LAA) thrombi. We sought to examine demographic and echocardiographic predictors of LAA thrombus in patients with persistent AF. METHODS AND RESULTS: One hundred and sixty-five patients in persistent AF (36 with LAA thrombus and 129 without thrombus) were studied. Demographic and cardiovascular risk factors were retrospectively examined. Transthoracic (TTE) and transoesophageal echocardiography (TOE) were performed to assess the size and function of the left ventricle (LV), left atrium (LA), LAA, and spontaneous echo contrast (SEC) in the LA and right atrium (RA). Univariate demographic predictors of LA thrombus included systolic blood pressure, ischaemic heart disease and congestive heart failure. Indexed LV mass and septal E' velocity on TTE and mean LAA emptying velocity and the presence of SEC in both the LA and RA on TOE were predictors of thrombus. In a multiple logistic regression analysis the only independent predictor of thrombus was indexed LV mass (P < 0.001). Receiver operator characteristic curve analysis also demonstrated that indexed LV mass had the highest area under the curve (AUC: 0.98). CONCLUSION: In the present study, increased LV mass was the strongest predictor of LAA thrombus in persistent AF. LA SEC and RA SEC were univariate predictors of LAA thrombus but did not add predictive value to a multivariate model including LV mass. This study highlights the importance of diagnosing and treating LV hypertrophy associated with persistent AF, which may reduce the risk of LAA thrombus and thrombo-embolic stroke.

Does the mode of exercise influence recovery of functional capacity in the early postoperative period after coronary artery bypass graft surgery? A randomized controlled trial.

OBJECTIVES: The purpose of this study was to compare the effectiveness of moderate-intensity stationary cycling and walking exercise programmes in the early postoperative period after first-time coronary artery bypass graft surgery. METHODS: In this prospective trial, 64 patients (57 men, 7 women, mean age = 66 ± 9 years) performed twice daily, moderate-intensity exercise sessions, of 10-min duration, from postoperative day 3 until discharge from hospital. Patients were randomly assigned to stationary cycling or walking exercise intervention groups. Preoperative and discharge functional exercise capacity and health-related quality of life were assessed using 6-min walk and cycle assessments and the SF-36 version 2.0 questionnaire. Compliance with exercise was calculated as the proportion of scheduled exercise sessions completed. RESULTS: There were no significant differences between intervention groups at hospital discharge for 6-min walk distance (cyclists: 402 ± 93 m vs walkers: 417 ± 86 m, P = 0.803), 6-min cycle work (cyclists: 15.0 ± 6.4 kJ vs walkers: 14.0 ± 6.3 kJ, P = 0.798) or health-related quality of life. There was no significant difference between intervention groups for postoperative length of hospital stay (P = 0.335). Compliance rates for intervention groups were cyclists: 185/246 (75%) scheduled exercise sessions completed vs walkers: 199/242 (82%) scheduled exercise sessions completed (P = 0.162). CONCLUSIONS: Stationary cycling provides a well-tolerated and clinically effective alternative to walking in the early postoperative period after coronary artery bypass graft surgery. The optimal frequency, intensity and duration of exercise in the early postoperative period require further investigation. (Clinical trials register: Australian New Zealand Clinical Trials Registry; identification number: ACTRN12608000359336; http://www.anzctr.org.au/trial_view.aspx?ID=82978).

Two-dimensional myocardial strain imaging detects changes in left ventricular systolic function immediately after anthracycline chemotherapy.

AIMS: The efficacy of anthracyclines is undermined by potential life-threatening cardiotoxicity. Cardiotoxicity is dependent upon several factors and the timing to its development is variable. Moreover, as adjuvant therapy with trastuzumab often follows, a close monitoring of cardiac function in those treated with anthracyclines is mandatory. Left ventricular ejection fraction (LVEF) by echocardiography is currently used for monitoring cardiotoxicity; however, LVEF has numerous limitations. Two-dimensional strain imaging may provide a more sensitive measure of altered LV systolic function, so the aim of the present study was to compare LVEF and LV systolic strain before and after anthracyclines. METHODS AND RESULTS: Fifty-two women with histologically confirmed breast cancer were prospectively studied. Echocardiographic LVEF (by Simpson's method), global and regional peak longitudinal, radial, and circumferential 2D systolic strain were measured 1 week before and 1 week after chemotherapy. Global and regional longitudinal LV systolic strain was significantly reduced after treatment; global longitudinal strain decreased from -17.7 to -16.3% (P < 0.01) with 48% of global measurements reduced by >10%. Global and regional radial LV systolic strain after treatment was also significantly reduced; global radial strain dropped from 40.5 to 34.5% (P < 0.01) with 59% of global measurements reduced by >10%. In contrast, no reduction in LVEF >10% after chemotherapy was observed. CONCLUSION: Reduced LV systolic strain immediately after anthracycline treatment may indicate early impairment of myocardial function before detectable change in LVEF.

Atrial strain rate is a sensitive measure of alterations in atrial phasic function in healthy ageing.

OBJECTIVE: Strain and strain rate measure local deformation of the myocardium and have been used to evaluate phasic atrial function in various disease states. The aim of this study was to define normal values for tissue Doppler-derived atrial strain measurements and examine age-related changes by decade in healthy individuals. METHODS: Transthoracic echocardiograms were performed on 188 healthy subjects. Tissue Doppler-derived strain and strain rate were measured from the apical four and two-chamber views of the left atrium, and global values were calculated as the mean of all segments. Measurements included peak systolic strain, systolic strain rate, early and late diastolic strain rate. Phasic left atrial volumes and fractions were calculated. Mitral inflow and tissue Doppler imaging were employed to estimate left ventricular diastolic function. RESULTS: A significant reduction in global systolic strain was observed from decade 6. Alterations in atrial strain rate were apparent from decade 5; systolic strain rate and early diastolic strain rate decreased, while late diastolic strain rate increased significantly. Changes in phasic atrial volume and function occurred in conjunction with age-related changes in left ventricular diastolic function. Importantly, age-related changes in global atrial systolic strain rate and early diastolic strain rate occurred a decade before corresponding changes in atrial phasic volume parameters. CONCLUSION: Atrial strain and strain rate can be used to quantify atrial phasic function and appear to be altered before traditional parameters with ageing. Strain analysis may therefore be more sensitive in detecting subclinical atrial dysfunction with alterations in strain rate parameters observed before traditional parameters.

The potential role of echocardiographic strain imaging for evaluating cardiotoxicity due to cancer therapy.

Refinements to conventional treatment and the development of new therapies have led to significant improvements in cancer survival. Yet, many frontline cancer treatments continue to be hindered by their significant side effects, amongst which cardiotoxicity is particularly important. Therefore, the focus of cancer management has changed; treatment is no longer aimed solely at overcoming malignancy, but emphasises early identification and treatment of potential side effects. In this regard, the cardiotoxic potential of certain anticancer agents mandate close monitoring of cardiac function, and the method of choice for monitoring is transthoracic echocardiography. Whilst this method has its limitations, a newer echocardiographic technique called myocardial strain imaging has the potential to detect early sub-clinical changes in cardiac function due to cardiotoxicity. Strain analysis has been the subject of several recent studies to evaluate its potential in monitoring cardiotoxicity, and this article reviews the recent literature and explores the potential role of myocardial strain imaging in cancer management and avenues for future research.

Clinical and electrocardiographic correlates of normal coronary angiography in patients referred for primary percutaneous coronary intervention.

This study sought to determine the prevalence as well as clinical and electrocardiographic correlates of patients referred for primary percutaneous coronary intervention (PCI) who had angiographically normal coronary arteries. Data for 690 consecutive patients with ST-elevation myocardial infarction (STEMI) referred for primary PCI within a metropolitan area health service were reviewed. Characteristics of patients with angiographically normal coronary arteries (n = 87; 13%) were compared with patients with angiographically shown culprit lesions (control group; n = 594). Nine patients with significant coronary disease, but no identifiable culprit lesion, were excluded. Electrocardiograms (ECGs) from both groups were reviewed by 2 cardiologists blinded to angiographic findings. Patients in the normal coronaries group were younger and had fewer risk factors. On expert review of ECGs, 55% of patients in the normal coronaries group had ST-elevation criteria for STEMI (vs 93% in the control group; p <0.001), but the ECG was considered consistent with a diagnosis of STEMI by both observers in only 33% (vs 92% in the control group; p <0.001). Left branch bundle block independently correlated with normal coronary arteries on multivariate analysis (odds ratio for STEMI 0.016, 95% confidence interval 0.004 to 0.064, p <0.001). The discharge diagnosis in the normal coronaries group was predominantly pericarditis (n = 72; 83%). In conclusion, the prevalence of angiographically normal coronary arteries in patients referred for primary PCI was 13%. Electrocardiographic correlation suggested that this can be reduced by adherence to conventional electrocardiographic criteria for STEMI diagnosis and review of ECGs by experienced clinicians.

Restrictive cardiomyopathy versus constrictive pericarditis: making the distinction using tissue Doppler imaging.

Although the primary cause of constrictive pericarditis is entirely different to that of restrictive cardiomyopathy, the two often present with very similar clinical findings. As such, making the distinction between the two is a diagnostic challenge. We report a case that highlights how tissue Doppler imaging may simplify the distinction between pericardial constriction and myocardial restriction.

Acute myocardial infarction complicated by LV free wall rupture: the benefits of echocardiography.

The recent increase in the number of cases of left ventricular free wall rupture being diagnosed before death and in the number of surgical repairs attempted is largely due to echocardiography. We report a case that highlights the value of echocardiography in the diagnosis and treatment of left ventricular free wall rupture following acute myocardial infarction.

Assessment, significance and mechanism of ventricular electrical instability after myocardial infarction.

The mechanism of reentrant tachycardia was established nearly a century ago, but the relationships between myocardial infarction and predisposition to sudden death were not unravelled until much later. In the latter half of the twentieth century many studies sought to ascertain what variables were predictive of death following myocardial infarction. Approximately one half of all deaths during the year following myocardial infarction are sudden and due to ventricular tachycardia (VT) or ventricular fibrillation (VF). We aimed to utilise non-invasive signal-averaging, along with programmed electrical stimulation of the heart, to determine whether one could predict spontaneous ventricular tachycardia and sudden death late after myocardial infarction. The sensitivity of ventricular electrical instablility (inducible ventricular tachycardia or fibrillation) as a predictor of instantaneous death or spontaneous VT was 86%, and the specificity was 83%. When other variables (delayed ventricular activation at signal-averaging, ejection fraction at gated heart pool scan, ventricular ectopic activity at ambulatory monitoring and exercise testing) were taken into account, inducible VT at electrophysiological study was the single best predictor of spontaneous VT and sudden cardiac death after myocardial infarction. The Westmead studies of Uther et al. in the decade or so from 1980 established programmed stimulation as the best predictor of sudden death after myocardial infarction. Subsequent studies by others have demonstrated a survival advantage of defibrillator implantation in patients with low ejection fraction (and inducible ventricular tachycardia) after myocardial infarction.

Mechanisms, prediction and treatment of ventricular tachyarrhythmias occurring late after myocardial infarction.

Studies from the 1980s, refined in the intervening years, have examined the milieu for ventricular tachycardia (VT) and ventricular fibrillation (VF) occurring late after acute myocardial infarction (AMI). The arrhythmogenic substrate appears to be patchy areas of fibrous tissue interdigitating with viable bundles of myocardium which have distorted orientation and tortuous interconnections. These promote conduction delay in sinus rhythm. Factors found to promote induction of VT rather than VF are longer conduction delay in sinus rhythm, larger infarct size, a more ragged infarct edge and longer ventricular extrastimulus coupling intervals. Predictors of spontaneous VT and VF late after AMI include inducible VT at electrophysiological studies (EPS), delayed conduction in sinus rhythm detected as late potentials on signal-averaged surface electrocardiogram (ECG), and low left ventricular ejection fraction (LVEF). Treatments of propensity for VT or VF after AMI include insertion of a defibrillator (ICD), which has the best track record, antiarrhythmic medication (less reliable), and ablation or excision of arrhythmogenic substrate (for refractory VT and VF).