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Background: Prognostication of congestive heart failure post-myocardial infarction (MI) is important for decision making. We sought of a head-to-head comparison between the prognostic implication of clinical, cardiopulmonary, and left ventricular (LV) function assessment., Methods: Retrospectively, 100 consecutive post-MI patients (MI history 1418+/-1668 days ago) were stratified by NYHA functional classification system, cardiopulmonary exercise testing (CPX) [oxygen consumption at maximal exercise (VO(2max)) and at the anaerobic threshold (VO(2AT)) resulting in the Weber classification], and LV function analysis by M-mode and two-dimensional echocardiography [LV end-diastolic and -systolic diameter index (LVDDI and LVSDI), shortening fraction (%D), and LV end-diastolic and -systolic volume index (EDVI and ESVI), LV ejection fraction (EF)]. Patients were controlled by phone call 1470+/-607 days later., Results: There was only a modest correlation between NYHA and Weber classes (r=0.402) and no correlation between VO(2max) and ESVI (r=0.080) nor between NYHA and ESVI (r=0.174). Several parameters (ESVI, LVDDI, LVSDI, %D) could discriminate NYHA classes to a higher significance (p=0.05; 0.0008; 0.0002; 0.04) than the Weber classes (n.s.; p=0.03; n.s.; n.s.). The following parameters could significantly differentiate quartiles in a log-rank analysis (Kaplan-Meier survival curves): NYHA classes (p=0.0001), Weber classes (p=0.069), EDVI (p=0.004), ESVI (p=0.0001), EF (p=0.002), LVDDI (p=0.002), LVSDI (p<0.001) and %D (p<0.001). Multivariate analysis isolated the following three parameters implying decreasing, independent prognostic information: NYHA classes (p=0.001), ESVI (p=0.003), and Weber classes (p=0.040)., Conclusions: In post-MI patients the thorough clinical assessment according the NYHA functional classification system implies higher prognostic information than more objective measures. This should be considered especially in primary care and should lessen the dependence on costly and expertise-dependent technical investigations.

Real-time myocardial contrast echocardiography (MCE) is a noninvasive perfusion imaging method, whereas technical and resolution problems impair its application in small animals. Hence, we investigated the feasibility of MCE in experimental cardiovascular set-ups involving healthy and infarcted myocardium in rats. Twenty-five male Wistar rats were examined under volatile anesthesia (2.5% isoflurane) with high-resolution conventional 2-D echocardiography (2DE) and real-time MCE (Sonos 7,500 with 15MHz-transducer, Philips Medical Systems, Andover, MA, USA) in short-axis view. Contrast agent (SonoVue, Bracco, Milan, Italy) was infused as a bolus into a sublingual vein. Background-subtracted contrast signal intensity (SI) was measured off-line in six end-systolic segments and fitted to an exponential curve (gamma variate). Derived peak SI was subsequently calculated and compared with wall motion and common functional measured quantities (left ventricular end-diastolic diameter [LVEDD], area shortening [AS]). Recordings were performed before and 14 days after left anterior descending (LAD) ligature. Infarction induced anterior wall motion abnormalities (WMA) in all animals (16 akinetic, 9 hypokinetic), increased LVEDD (9.1 +/- 0.6 vs. 7.9 +/- 0.6 mm, p < 0.001), reduced AS (36.1 +/- 10.0 vs. 59.5 +/- 4.1%, p < 0.001) and reduced anterior segmental SI (0.4 +/- 0.4 dB akinetic / 1.7 +/- 1.7 dB hypokinetic vs. 15.8 +/- 10.9 dB preinfarct, p < 0.001 / p < 0.001). Segmental SI in normokinetic segments remained unchanged. Area at risk (perfusion defect) correlated well with WMA (r = 0.838). These data confirmed high-resolution real-time MCE as a rational tool for assessing myocardial perfusion of Wistar rats. It may therefore be a useful diagnostic tool for in-vivo cardiovascular research in small animals.

Background/aims: Mitral regurgitation (MR) following myocardial infarction (MI) may be a (sub)acute complication which independently predicts reduced survival. We sought to evaluate the chronic development of MR as potential consequence of left-ventricular (LV) remodelling, the latter being a long-term process., Methods and Results: Retrospectively, 103 post-MI patients were included according to a standardised Doppler echocardiogram <3 months following MI (20 +/- 25 days post-MI) and a follow-up examination >6 months after the first examination (5.1 +/- 3.1 years post-MI). Patients were clinically followed up for 7.6 +/- 2.7 years. Group I patients were defined as those showing new development or deterioration in one of three grades of MR, and group II those without this criterion (MR grade acute 0.17 vs. 0.27, p = 0.7, and chronic 1.53 vs. 0.19, p < 0.0001). Patient characteristics were similar in respect of age, gender, size and location of infarction. However, group I patients had coronary artery disease with more vessels involved. With regard to echocardiographic parameters of significantly enlarged LV chamber size in group I vs. group II, the significant decrease in LV performance was more pronounced and occurred concomitant with a higher degree of symptomatic congestive heart failure and greater need for heart failure medications in group I. Mortality in group I patients was 39 versus 9% in group II patients (p = 0.0002), approximating an odds ratio of 6.4697 (95% confidence interval: 2.211-18.931)., Conclusion: First of all, this retrospective study indicates that MR may be detected in patients after MI during a long-term follow-up most probably due to geometric distortions of LV remodelling resulting in a significantly higher mortality. Since this process is known to become irreversible at a certain point, serial echocardiography may help to detect MR in post-MI patients and thus pave the way for appropriate treatment., (2007 S. Karger AG, Basel)

The concept of regenerating diseased myocardium by implantation of tissue-engineered heart muscle is intriguing, but convincing evidence is lacking that heart tissues can be generated at a size and with contractile properties that would lend considerable support to failing hearts. Here we created large (thickness/diameter, 1-4 mm/15 mm), force-generating engineered heart tissue from neonatal rat heart cells. Engineered heart tissue formed thick cardiac muscle layers when implanted on myocardial infarcts in immune-suppressed rats. When evaluated 28 d later, engineered heart tissue showed undelayed electrical coupling to the native myocardium without evidence of arrhythmia induction. Moreover, engineered heart tissue prevented further dilation, induced systolic wall thickening of infarcted myocardial segments and improved fractional area shortening of infarcted hearts compared to controls (sham operation and noncontractile constructs). Thus, our study provides evidence that large contractile cardiac tissue grafts can be constructed in vitro, can survive after implantation and can support contractile function of infarcted hearts.

Objective: Myocardial longitudinal shortening after aortic valve closure (postsystolic shortening [PSS]) is considered a marker of pathology with diagnostic potential. However, PSS can also occur in healthy subjects. We, therefore, investigated the occurrence and characteristics of PSS in control subjects and patients, and how to distinguish normality from disease., Methods: In 20 young control subjects, 10 older control subjects, 30 patients with acute myocardial infarction (acute ischemia), and 10 patients with postischemic myocardial scar, longitudinal myocardial deformation was measured with Doppler tissue strain rate (SR) imaging. Segmental SR and strain were visually and quantitatively analyzed and compared., Results: In young control subjects, PSS was found in 98 of 313 segments (31%) and showed gaussian distribution (median 1.3%). During ejection time, median peak SR was -1.4 s(-1) and median strain -16.6%. In older control subjects, parameters differed only slightly. In acutely ischemic and scarred myocardium, both systolic strain and SR were significantly reduced or inverted. In disease, PSS occurred significantly more often (78% and 79%, respectively), was significantly higher in magnitude, and its peak occurred later than in young and older control subjects., Conclusion: PSS is a normal finding in healthy subjects occurring in approximately one-third of myocardial segments and, thus, is not always a marker of disease. Our data indicate that pathologic PSS can be detected by coexisting reduction in systolic strain and, second, by exceeding a postsystolic strain magnitude cutoff.

Myocardial viability within the infarct zone is an important determinant for left ventricular (LV) function recovery after interventional coronary revascularization. Echocardiographic techniques are highly valuable in identifying hibernation, especially in conjunction with dobutamine titration. Low doses may detect the inotropic reserve by significant enhancement of segmental wall motion abnormalities while high doses may surpass the ischemic threshold and wall motion deteriorates (biphasic response). According to the Task Forces on Clinical Application of Echocardiography by the American Heart Association (AHA) in cooperation with the American College of Cardiology (ACC), dobutamine echocardiography (DE) is officially recommended for the purpose of clincial decision making in respect of revascularization therapies (whether during the subacute infarct period or especially in chronic LV dysfunction due to coronary artery disease (CAD)). New methods such as strain rate imaging implemented in DE are on the way to give us quantitative measures of the amount of viability.(J Interven Cardiol 2004;17:349–355) [ABSTRACT FROM AUTHOR]