Ventricular Wall Motion Index Research Articles

Long-term follow up of left ventricular remodeling in ST segment myocardial infarction patients after primary percutaneous coronary intervention

Introduction The adaptive reaction known as left ventricular remodeling after ST-elevation myocardial infraction (STEMI) involves both the infarct zone and remote zones, and it lasts for at least 2 years after STEMI. In STEMI patients having primary percutaneous coronary intervention (PPCI), this study was conducted to look at long-term consequences of left ventricular remodeling. Patients and methods Ninety-three patients were successfully treated by primary PCI more than 2 years ago at Assiut University Heart Hospital were enrolled in this study. Detailed history, complete general examination and local cardiac examination were done. Electrocardiography, two-dimensional echocardiography before primary PCI, at discharge and 6 months after PPCI, coronary angiographic and PPCI data from patient admission sheet. Patients were examined by transthoracic 2DE using Phillips ie33 ultrasound system device. Results Thirty-six (38.7%) patients were determined to have left ventricular remodeling when their left ventricular end diastolic volume index increased by more than 20%, compared with 57 (61.3%) patients who did not. Mean age of patients 56.31 ± 11.11 years and mean overall duration of follow up was 3.69 ± 0.45 years. The long-term predictors of left ventricular remodeling were: extensive anterior MI (P < 0.001), left anterior descending as infarct-related artery (P = 0.03), left ventricular end systolic volume index (P = 0.04) and wall motion index (P < 0.001). Discussion Patients who had extensive anterior MI, a wall motion score index more than 1.5, and left anterior descending as infarct-related artery were seen as having a high probability of LV remodeling following PPCI. Only wall motion score index more than 1.5 and extensive anterior MI were independent indicators of LV remodeling following PPCI.

Correlation of Admission Time Blood Glucose, Left Ventricular Function and Regional Wall Motion Index with Occurrence of In-hospital Major Adverse Cardiac Events in Acute Coronary Syndrome

Correlation of Admission Time Blood Glucose, Left Ventricular Function and Regional Wall Motion Index with Occurrence of In-hospital Major Adverse Cardiac Events in Acute Coronary Syndrome

Pro-Substance P for Evaluation of Risk in Acute Myocardial Infarction

BackgroundPro-substance P (ProSP) is a stable surrogate marker for labile substance P, which has pro-inflammatory effects, increases platelet aggregation and clot strength, and reduces fibrinolysis. ObjectivesThis study assessed whether ProSP was associated with poor prognosis after acute myocardial infarction (AMI) to identify novel pathophysiological mechanisms. MethodsProSP was measured in 1,148 AMI patients (825 men, mean age 66.2 ± 12.8 years). Endpoints were major adverse cardiac events (composite of death, reinfarction, and heart failure [HF] hospitalization), death/reinfarction, and death/HF. GRACE (Global Registry of Acute Coronary Events) scores were compared with ProSP for death and/or reinfarction at 6 months. ResultsDuring 2-year follow-up, there were 140 deaths, 112 HF hospitalizations, and 149 re-AMI. ProSP levels were highest on the first 2 days after admission and related to estimated glomerular filtration rate, age, history of diabetes, ischemic heart disease or hypertension, Killip class, left ventricular wall motion index, and sex. Multivariate Cox regression models showed ProSP level was a predictor of major adverse events (hazard ratio [HR]: 1.30; 95% confidence interval [CI]: 1.10 to 1.54; p < 0.002), death and/or AMI (HR: 1.42; 95% CI: 1.20 to 1.68; p < 0.0005), death and/or HF (HR: 1.38; 95% CI: 1.14 to 1.67; p < 0.001). ProSP levels with GRACE scores were independent predictors of 6-month death and/or reinfarction (p < 0.0005 for both). ProSP-adjusted GRACE scores reclassified patients significantly (overall category-free net reclassification improvement of 31.6 (95% CI: 14.3 to 49.0; p < 0.0005) mainly by down-classifying those without endpoints. ConclusionsProSP levels post-AMI are prognostic for death, recurrent AMI, or HF, and they improve risk prediction of GRACE scores, predominantly by down-classifying risk in those without events.

Proenkephalin and Prognosis After Acute Myocardial Infarction

The goal of this research was to assess the prognostic value of proenkephalin (PENK) levels in acute myocardial infarction (AMI) by using N-terminal pro-B-type natriuretic peptide and Global Registry of Acute Coronary Events (GRACE) scores as comparators and to identify levels that might be valuable in clinical decision making. PENK is a stable analyte of labile enkephalins. Few biomarkers predict recurrent AMI. We measured PENK in 1,141 patients (820 male subjects; mean age 66.2 ± 12.8 years) with AMI. Endpoints were major adverse events (composite of death, myocardial infarction [MI], and heart failure [HF] hospitalization) and recurrent MI at 2 years. GRACE scoring was used for comparisons with PENK for the death and/or MI endpoint at 6 months. During follow-up, 139 patients died, and there were 112 HF hospitalizations and 149 recurrent AMIs. PENK levels were highest on admission and were related to estimated glomerular filtration rate, left ventricular wall motion index, sex, blood pressure, and age. Multivariable Cox regression models found that the PENK level was a predictor of major adverse events (hazard ratio [HR]: 1.52 [95% confidence interval (CI): 1.19 to 1.94]), death and/or AMI (HR:1.76 [95% CI: 1.34 to 2.30]), and death and/or HF (HR: 1.67 [95% CI: 1.24 to 2.25]) (all comparisons p< 0.001), as well as recurrent AMI (HR: 1.43 [95% CI: 1.07 to 1.91];p< 0.01). PENK levels were independent predictors of 6-month death and/or MI compared with GRACE scores. PENK-adjusted GRACE scores reclassified patients significantly (overall category-free net reclassification improvement [>0] of 21.9 [95% CI: 4.5 to 39.4]; p< 0.014). PENK levels<48.3 pmol/l and >91 pmol/l detected low- and high-risk patients, respectively. PENK levels reflect cardiorenal status post-AMI and are prognostic for death, recurrent AMI, or HF. Cutoff values define low- and high-risk groups and improve risk prediction of GRACE scores.

Prognostic value of biological markers in myocardial infarction patients

The aim of this study was to compare the prognostic value of matrix metalloproteinase-3 and -9, and NT-pro-natriuretic peptide for fatal and nonfatal complications in Q-wave myocardial infarction patients in the acute and postinfarction periods. 85 men and women with documented Q-wave myocardial infarction were observed for 1 year after hospitalization. Clinical endpoints were identified through the hospital patient-tracking system, with a review of medical records for each recorded endpoint. Left ventricular ejection fraction and wall motion index were calculated. Measurements of matrix metalloproteinases and NT-pro-natriuretic peptide were performed by an enzyme-linked immunosorbent assay. A cutoff value of 9.7 ng·mL(-1) for matrix metalloproteinase-3 showed the best discriminatory power (sensitivity = 77.8%, specificity = 90.8%). The optimal cutoff value of matrix metalloproteinase-9 was 18.1 ng·mL(-1) (sensitivity, 70.5%; specificity, 75%), and the cutoff for NT-pro-natriuretic peptide was 885 pmol·L(-1) (sensitivity, 58%; specificity, 68.6%). Matrix metalloproteinase-3 and -9 were strongly related with a positive prognostic value of 70% (sensitivity and specificity, 84% and 82%, respectively). These data may be helpful for further stratification of patients into cardiovascular mortality risk groups.

Protective effect of Chinese herbs for supplementing qi, nourishing yin and activating blood circulation on heart function of patients with acute coronary syndrome after percutaneous coronary intervention

To investigate the effects of Chinese herbs for supplementing qi, nourishing yin and activating blood circulation on heart function of patients with acute coronary syndrome (ACS) after successful percutaneous coronary intervention (PCI). One hundred patients with ACS after successful PCI were randomly assigned to a Western medicine (WM) treatment group (WMG) and a combined treatment group (CMG) treated by Chinese herbs for supplementing qi, nourishing yin and activating blood circulation, besides Western medicine treatment, with 50 cases in each group. Both treatment courses were 6 months. The followup was scheduled at baseline, 6 months and 1 year after PCI, and New York Heart Association (NYHA) functional class, Chinese medicine (CM) symptom scores, blood stasis syndrome scores, and major adverse cardiovascular events (MACE) were observed, serum levels of N-terminal pro-brain natriuretic peptide (NT-proBNP) and hyper-sensitivity C-reactive protein (Hs-CRP) were measured, an echocardiogram was conducted to examine left ventricular ejection fraction (LVEF), left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), inter-ventricular septal thickness (IVST), left ventricular posterior wall thickness (LVPWT), and ventricular wall motion index (VWMI). Compared with the baseline, LVEF significantly increased (P<0.01), and CM symptom scores, blood stasis syndrome scores, VWMI, LVEDV, LVESV, NT-proBNP, and Hs-CRP all decreased (P<0.01) in both groups at 6 months and at 1 year after PCI. There were no significant differences in all the above parameters at 1 year vs those at 6 months after PCI (P>0.05). VWMI, LVEDV, LVESV, NT-proBNP, Hs-CRP, LVEF, and CM symptom and blood stasis syndrome scores were all improved obviously in CMG than those in WMG (P<0.05 or P<0.01) at 6 months and at 1 year after PCI. There were no significant differences in NYHA functional class between CMG and WMG at different follow-up timepoints; it was notable that value was 0.054 when comparing the cases of NYHA functional class between the two groups at 1-year follow-up. During the 1-year follow-up, 3 MACE and 11 MACE occurred in CMG and WMG, respectively; the MACE rate in CMG was lower than that in WMG (6% vs 22%, P<0.05). Chinese herbs for supplementing qi, nourishing yin and activating blood circulation could improve heart function, reduce the CM symptom scores and blood stasis syndrome scores, and decrease the incidence of MACE in patients with ACS after successful PCI.

Randomized Comparison of Distal Protection Versus Conventional Treatment in Primary Percutaneous Coronary Intervention: The Drug Elution and Distal Protection in ST-Elevation Myocardial Infarction (DEDICATION) Trial

The purpose of this study was to evaluate the use of distal protection during percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction (STEMI) in native coronary vessels. Embolization of material from the infarct-related lesion during PCI may result in impaired myocardial perfusion and worsen the prognosis. Previous attempts to protect the microcirculation during primary PCI have had conflicting results. We randomly assigned 626 patients with STEMI referred within 12 h to have PCI performed with (n = 312) or without (n = 314) distal protection. The primary end point was complete (>or=70%) ST-segment resolution detected by continuous ST-segment monitoring. Blood levels of troponin-T and creatine kinase-MB were monitored before and after the procedure, and echocardiographic determination of the left ventricular wall motion index (WMI) was performed before discharge. Patients were well matched in terms of demographic and angiographic baseline characteristics. There was no significant difference in the occurrence of the primary end point (76% vs. 72%, p = 0.29), no difference in maximum troponin-T (4.8 microg/l and 5.0 microg/l, p = 0.87) or maximum creatine kinase-MB (185 microg/l and 184 microg/l, p = 0.99), and no difference in median WMI (1.70 vs. 1.70, p = 0.35). The rate of major adverse cardiac and cerebral events (MACCE) 1 month after PCI was 5.4% with distal protection and 3.2% with conventional treatment (p = 0.17). The routine use of distal protection by a filterwire system during primary PCI does not seem to improve microvascular perfusion, limit infarct size, or reduce the occurrence of MACCE.

Ventricular remodeling following acute myocardial infarction: The role of altered collagen homeostasis

Ventricular remodeling following myocardial infarction, characterized by detrimental changes on ventricular size, shape and function, is considered to be one of the most powerful predictors of adverse outcomes after myocardial infarction [1,2]. Recently, McGavigan et al. [3] have evaluated the role of impaired collagen homeostasis in predicting the development of early ventricular remodeling following acute myocardial infarction. Fifty-one patients with acute myocardial infarction have been included in this study. Twenty-three of these patients had normal left ventricular wall motion index and 28 have had abnormal wall motion index. C-propeptide for type-I collagen (PICP) andC-telopeptide for type-I collagen (CITP) have been measured as the markers of collagen synthesis and degradation, respectively. Patients who manifested early left ventricular remodeling following acute myocardial infarction have increased degradation and reduced synthesis of collagen, favoring net collagen breakdown. Both groups with normal and abnormalwall motion index have shown to have increased in PICP and CITP over time. However mean admission of CITP levels, indicating collagen degradation, has been detected to be significantly higher in patients with abnormal wall motion index. In contrary, admission of PICP levels, indicating collagen synthesis, has been shown to be significantly lower in abnormal wall motion index group. In addition admission of CITP levels had a positive correlation with wall motion index. CITPN3.2 ng/ml has been reported to

Matrix Metalloproteinase-9 Is a Marker of Heart Failure After Acute Myocardial Infarction

Background Matrix metalloproteinases (MMPs) have been associated with the development of left ventricular remodeling after myocardial infarction (MI). We sought to determine whether peripheral levels of MMPs can be used as a risk marker for the development of congestive heart failure (CHF) after acute MI. Methods and Results Plasma levels of MMP-2, MMP-9, C-reactive protein (hs-CRP), tumor necrosis factor-α (TNF-α), and pro-brain natriuretic peptide (pro-BNP) were measured in 109 consecutive patients with acute MI treated with primary mechanical reperfusion. Echocardiographic assessment of left ventricular wall motion index was performed during admission. Patients were followed for the development of CHF. Left ventricular function and volumes were determined after 2 years with radionuclide ventriculography. During 2-year follow-up, 15 patients developed congestive heart failure (CHF). Using multivariate analysis, MMP-9 levels were the only circulating factor predictive of late onset CHF. Patients who had high MMP-9 levels had a significant risk of late onset CHF (OR of 6.5, P ≤ .006) and left ventricular remodeling (ΔEF = −9%, P = .03, and Δend-diastolic volume = +13 mL, P = .03). MMP-2, TNF-α, hs-CRP, creatine kinase, and pro-BNP were not predictive of late onset CHF. Conclusion MMP-9 levels may hold prognostic significance in MI patients.

The Reliability of Echocardiographic Left Ventricular Wall Motion Index to Identify High‐Risk Patients for Multicenter Studies

To study whether the use of echocardiographic left ventricular (LV) wall motion index (WMI) is a dependable parameter for identifying patients with LV dysfunction to be enrolled in multicenter trials. Videotaped echocardiographic examinations from 200 randomly selected patients that were screened for inclusion into the DIAMOND-CHF and DIAMOND-MI trials were reevaluated by an external expert echocardiographer. WMI was calculated using the 16-segment LV model. The external echocardiographer systematically found lower values of WMI than the core laboratory. The average difference in WMI was 0.18 (SD: 0.33) in the DIAMOND-CHF trial and 0.09 (SD: 0.33) in the DIAMOND-MI trial. The difference in WMI exceeded 0.33 in 34% of the patients in both trials. The cutoff value for inclusion into the DIAMOND trials was WMI < or = 1.2. There was an agreement on WMI dichotomized to below or above 1.2 in 82% of the patients in both trials (kappa coefficient 0.66 for the DIAMOND-CHF and 0.55 for the DIAMOND-MI). Despite substantial interlaboratory variation in WMI in individual patients and a systematic lower WMI score by the external echocardiographer there was an acceptable overall agreement for identifying patients with severe impairment of LV function. This not only underscores the value of LV-WMI as a useful tool for selecting high-risk patients to be included in multicenter studies but also serves to warn against the use of rigid cutoff values for WMI in the treatment of individual patients.

Plasma MMP-9 and MMP-2 following acute myocardial infarction in man: correlation with echocardiographic and neurohumoral parameters of left ventricular dysfunction

Background Left ventricular dilatation and elevated plasma natriuretic peptide levels predict adverse prognosis and the development of congestive heart failure after myocardial infarction. Altered matrix metalloproteinase (MMP) activity has been implicated in the structural changes associated with development of heart failure after myocardial injury. The aims of this study were to investigate plasma MMP-2, MMP-9, and tissue inhibitor of metalloproteinase (TIMP)-1 concentrations following acute myocardial infarction and their relationships with measures of left ventricular function. Methods and results Plasma MMP-2, MMP-9, TIMP-1, and N-terminal proBNP (N-BNP) were quantified on 5 consecutive days in 60 patients with acute myocardial infarction (39 anterior). N-BNP was measured on day 3. Echocardiographic assessment of left ventricular wall motion index and volumes was performed during admission and 6 weeks later. Plasma MMP-9 showed peaks on days 1 and 4. MMP-2 levels, similar on each day, were higher after inferior myocardial infarction. Plasma MMP-2 showed strong, inverse correlation with left ventricular volumes during and after admission. Plasma MMP-9 correlated directly with N-BNP ( P = .022) and inversely with wall motion index during admission ( P = .05). TIMP-1 levels were higher after anterior (1269, 870-1466 ng/mL) compared with inferior (1183, 856-1419 ng/mL, P = .05) acute myocardial infarction and fell from day 1 through 5 ( P < .0005). Conclusion Plasma MMP-9 concentration correlates with neurohormonal and echocardiographic measures of left ventricular dysfunction after myocardial infarction. Higher left ventricular volumes are associated with lower plasma MMP-2 concentrations. Circulating MMP concentrations may provide insights into left ventricular remodeling after acute myocardial infarction.

Ischemic and viable myocardium in patients with Non–Q-Wave or Q-Wave myocardial infarction and left ventricular dysfunction: A clinical study using positron emission tomography, echocardiography, and electrocardiography

ObjectivesWe investigated whether patients with non–Q-wave myocardial infarction (NQMI) have more ischemic viable myocardium (IVM) than patients with Q-wave myocardial infarction (QMI). BackgroundNon–Q-wave myocardial infarction is associated with higher incidences of cardiac events than QMI, suggesting more myocardium at risk in NQMI. MethodsTo identify myocardial ischemia, hibernation, and scar, the resting and stress 82rubidium perfusion and F-18 fluorodeoxyglucose metabolic positron emission tomographic imaging (PET) was performed in 64 consecutive patients with NQMI (n = 21) or QMI (n = 43). Echocardiography was performed for assessment of left ventricular function and wall motion index (WMI). The relationships between PET, echocardiographic, and electrocardiographic findings were analyzed. ResultsThere were no significant differences in left ventricular ejection fraction (LVEF) between NQMI and QMI groups (28 ± 10% vs. 25 ± 11%, p > 0.05). Ischemic and viable myocardium was more common in NQMI than in QMI (91% vs. 61%, p < 0.05). The total amount of IVM was significantly higher in NQMI than in QMI (6.5 ± 5.2 vs. 2.9 ± 2.8 segments, p < 0.001). Neither the number of Q waves, residual ST-segment depression of ≥0.5 mm or elevation of ≥1 mm, nor LVEF and WMI were significant predictors for IVM. Wall motion index correlated with scar segments (r = 0.54, p < 0.001) and LVEF (r = −0.67, p < 0.001). ConclusionsIschemic and viable myocardium is common in patients with NQMI and left ventricular dysfunction, suggesting that aggressive approaches should be taken to salvage the myocardium at risk in such patients.

Profile of plasma N-terminal proBNP following acute myocardial infarction; correlation with left ventricular systolic dysfunction.

The aims of this study were to describe the temporal pattern of plasma N-terminal pro-brain natriuretic peptide, to examine the optimum time of sampling and to compare plasma N-terminal pro-brain natriuretic peptide to clinical criteria in terms of identification of impaired left ventricular systolic function following acute myocardial infarction. Measurements of N-terminal pro-brain natriuretic peptide were made in 60 patients at 14-48 h, 49-72 h, 73-120 h, 121-192 h following myocardial infarction and at 6 weeks in survivors. Left ventricular wall motion index was assessed during hospitalization (WMI-1) and at 6 weeks (WMI-2). N-terminal pro-brain natriuretic peptide levels were elevated at all time points, to a greater extent in anterior compared to inferior infarction (P < 0.05). A biphasic profile of plasma concentration was observed in anterior infarction with peaks at 14-48 h and 121-192 h. This was sustained at 6 weeks. N-terminal pro- brain natriuretic peptide at 73-120 h was the best independent predictor of WMI-1 (P < 0.005). N-terminal pro-brain natriuretic peptide was higher at all times in patients who received ACE inhibitor therapy compared to those who did not (P < 0.005). N-terminal pro-brain natriuretic peptide at 73-120 h (R(2) = 17.7%, P = 0.005) and previous myocardial infarction (R(2) = 5.3%, P < 0.05) were independent predictors of poor outcome (WMI-2 < or = 1.2 or death by 6 weeks). A biphasic pattern of plasma N-terminal pro-brain natriuretic peptide is seen after anterior myocardial infarction. Plasma level is strongly correlated to wall motion index soon after and remote from acute myocardial infarction. Plasma N-terminal pro-brain natriuretic peptide measured later in hospitalization better predicts poor outcome following myocardial infarction than when it is measured in the immediate post infarction period.

Elevated circulating cardiotrophin-1 in heart failure: relationship with parameters of left ventricular systolic dysfunction

Cardiotrophin-1 (CT-1) is a cytokine that has been implicated as a factor involved in myocardial remodelling. The objective of the present study was to establish the relationship between circulating levels of CT-1 and measures of left ventricular size and systolic function in patients with heart failure. We recruited 15 normal subjects [six male; median age 60 years (range 30–79 years)] and 15 patients [11 male; median age 66 years (range 43–84 years)] with a clinical diagnosis of heart failure and echocardiographic left ventricular systolic dysfunction (LVSD). Echocardiographic variables (left ventricular wall motion index, end-diastolic and -systolic volumes, stroke volume, fractional shortening) and plasma CT-1 levels were determined. In patients with LVSD [median wall motion index 0.6 (range 0.3–1.4)], CT-1 was elevated [median 110.4 fmol/ml (range 33–516 fmol/ml)] compared with controls [wall motion index 2 in all cases; median CT-1 level 34.2 fmol/ml (range 6.9–54.1 fmol/ml); P &lt; 0.0001]. Log CT-1 was correlated with log wall motion index (r = -0.76, P &lt; 0.0001), log left ventricular end-systolic volume (r = 0.54, P &lt; 0.05), stroke volume (r = -0.60, P = 0.007) and log fractional shortening (r = -0.70, P = 0.001). In a multivariate model of the predictors of log wall motion index, the only significant predictor was log CT-1 (R2 = 56%, P = 0.006). This is the first assessment of the relationship between plasma CT-1 levels and the degree of LVSD in humans, and demonstrates that CT-1 is elevated in heart failure in relation to the severity of LVSD.

Elevated circulating cardiotrophin-1 in heart failure: relationship with parameters of left ventricular systolic dysfunction

Cardiotrophin-1 (CT-1) is a cytokine that has been implicated as a factor involved in myocardial remodelling. The objective of the present study was to establish the relationship between circulating levels of CT-1 and measures of left ventricular size and systolic function in patients with heart failure. We recruited 15 normal subjects [six male; median age 60 years (range 30-79 years)] and 15 patients [11 male; median age 66 years (range 43-84 years)] with a clinical diagnosis of heart failure and echocardiographic left ventricular systolic dysfunction (LVSD). Echocardiographic variables (left ventricular wall motion index, end-diastolic and -systolic volumes, stroke volume, fractional shortening) and plasma CT-1 levels were determined. In patients with LVSD [median wall motion index 0.6 (range 0.3-1.4)], CT-1 was elevated [median 110.4 fmol/ml (range 33-516 fmol/ml)] compared with controls [wall motion index 2 in all cases; median CT-1 level 34.2 fmol/ml (range 6.9-54.1 fmol/ml); P<0.0001]. Log CT-1 was correlated with log wall motion index (r=-0.76, P<0.0001), log left ventricular end-systolic volume (r=0.54, P<0.05), stroke volume (r=-0.60, P=0.007) and log fractional shortening (r=-0.70, P=0.001). In a multivariate model of the predictors of log wall motion index, the only significant predictor was log CT-1 (R(2)=56%, P=0.006). This is the first assessment of the relationship between plasma CT-1 levels and the degree of LVSD in humans, and demonstrates that CT-1 is elevated in heart failure in relation to the severity of LVSD.

An immunoluminometric assay for N-terminal pro-brain natriuretic peptide: development of a test for left ventricular dysfunction

Measurement of plasma levels of brain natriuretic peptide (BNP) has been used to assess left ventricular dysfunction and prognosis. Levels of the N-terminus of the precursor of BNP (NTproBNP) have been reported to be elevated to a greater extent than BNP in left ventricular dysfunction. We have devised a non-radioactive sensitive and specific assay for NT-proBNP based on a competitive ligand binding principle. The chemiluminescent label 4-(2-succinimidyloxycarbonylethyl)phenyl-10-methylacridinium 9-carboxylate fluorosulphonate was used to label peptides representing domains in the middle and C-terminal sections of NT-proBNP. Assay of the C-terminal section of NT-proBNP (amino acids 65‐76) in patients with proven left ventricular dysfunction [left ventricular wall motion index median 0.9 (range 0.3‐1.4)] revealed elevated values [median 639 (386‐911) fmol/ml] compared with normal controls [left ventricular wall motion index of 2 in all, NT-proBNP median 159 (120‐245) fmol/ml, P ! 0.001]. Measurement of the middle section of NT-proBNP (amino acids 37‐49) was not a discriminating test. It is thus possible to derivatize small peptides with a methyl acridinium label and preserve immunodetection with specific antibodies. Such methodology may allow non-radioactive immunoluminometric assays to be devised.

An immunoluminometric assay for N-terminal pro-brain natriuretic peptide: development of a test for left ventricular dysfunction

Measurement of plasma levels of brain natriuretic peptide (BNP) has been used to assess left ventricular dysfunction and prognosis. Levels of the N-terminus of the precursor of BNP (NT-proBNP) have been reported to be elevated to a greater extent than BNP in left ventricular dysfunction. We have devised a non-radioactive sensitive and specific assay for NT-proBNP based on a competitive ligand binding principle. The chemiluminescent label 4-(2-succinimidyloxycarbonylethyl)phenyl-10-methylacridinium 9-carboxylate fluorosulphonate was used to label peptides representing domains in the middle and C-terminal sections of NT-proBNP. Assay of the C-terminal section of NT-proBNP (amino acids 65-76) in patients with proven left ventricular dysfunction [left ventricular wall motion index median 0.9 (range 0.3-1.4)] revealed elevated values [median 639 (386-911) fmol/ml] compared with normal controls [left ventricular wall motion index of 2 in all, NT-proBNP median 159 (120-245) fmol/ml, P<0.001]. Measurement of the middle section of NT-proBNP (amino acids 37-49) was not a discriminating test. It is thus possible to derivatize small peptides with a methyl acridinium label and preserve immunodetection with specific antibodies. Such methodology may allow non-radioactive immunoluminometric assays to be devised.

Effect of delayed percutaneous transluminal coronary angioplasty of occluded coronary arteries after acute myocardial infarction

Whether angioplasty of occluded vessels after myocardial infarction may have beneficial effects on left ventricular function remains unknown. Patients with a first myocardial infarction and thrombolytic therapy who had an occluded infarct-related vessel at delayed coronary angiography were referred systematically for an elective coronary angioplasty performed between 3 and 4 weeks after the myocardial infarction. All patients underwent stress-redistribution-reinjection thallium-201 single-photon emission computed tomography for myocardial viability assessment. Prior angioplasty, a quantitative evaluation of global and regional left ventricular function, was performed. The study group consisted of 38 patients (aged 57 ± 10 years); 18 had anterior wall infarctions and 20 inferior wall infarctions, but before angioplasty 3 had a patent artery and were excluded. Angioplasty was successful in 30 patients. At follow-up 13 patients (43%) had an occluded coronary artery. In contrast with patients with an occluded coronary artery at follow-up, those with a patent coronary artery had no left ventricular enlargement and had an improvement in both left ventricular ejection fraction (from 48 ± 9% to 52 ± 9.8%, p = 0.002) and regional wall motion index (Δ = +0.95 SD, p < 0.01). In patients with a patent vessel at follow-up, there was a positive correlation between the number of myocardial viable segments and improvement of the infarct zone wall motion (r = 0.52; p = 0.035), and the number of necrotic segments at baseline was positively correlated to the 4-month changes in end-diastolic volume indexes (r = 0.6; p = 0.04). Thus, elective revascularization of occluded coronary arteries with viable myocardium after myocardial infarction improves left ventricular function and lessens remodeling if the artery remains patent during follow-up.

Two-dimensional echocardiography and Doppler color flow mapping in the diagnosis and prognosis of ventricular septal rupture.

Doppler color flow mapping in conjunction with two-dimensional echocardiography was used to evaluate ventricular septal rupture after myocardial infarction (seven anterior and eight inferior) in 15 patients and to correlate these findings with cardiac catheterization and surgical or autopsy data. Ventricular septal rupture was diagnosed by turbulent flow traversing the ventricular septum. The direction and velocity of shunt flow was determined by color M-mode and conventional Doppler methods. In all patients, Doppler color flow mapping correctly defined the site of septal rupture, which occurred at areas of discordant septal wall motion or "hinge points" (six posterior inlet, three anterior inlet, and six apical trabecular septum). Each of three patients with moderate tricuspid regurgitation and three of four patients with right-to-left shunting during diastole died, and all had an elevated right ventricular end-diastolic pressure. Right ventricular wall motion index was significantly higher in the patients who died compared with those who survived (mean +/- SEM; 2.8 +/- 0.2 vs. 2.0 +/- 0.2, p = 0.012), but there was no difference in left ventricular wall motion index. The rupture size measured by Doppler color flow imaging (1.7 +/- 0.1 cm) correlated with the size determined during surgery or autopsy (1.8 +/- 0.2 cm, r = 0.68, p = 0.022) and the pulmonic-to-systemic shunt flow ratio by cardiac catheterization (2.4:1 +/- 0.3, r = 0.74, p = 0.004). Color-guided continuous-wave Doppler estimates of right ventricular systolic pressure (47 +/- 2 mm Hg) correlated with cardiac catheterization measurements (48 +/- 3 mm Hg, r = 0.90, p = 0.0002).(ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamically important right ventricular infarction: follow-up evaluation of right ventricular systolic function at rest and during exercise with radionuclide ventriculography and respiratory gas exchange.

The prognosis and recovery of right ventricular systolic function in patients with hemodynamically documented right ventricular myocardial infarction (RVMI) is unclear. Therefore 27 patients who met hemodynamic criteria for RVMI were followed for at least 1 year. Four patients died within 1 year and 23 survived. Postmortem examination performed in three of the four patients showed extensive infarction of the right and left ventricles. Survivors underwent early and late follow-up resting radionuclide ventriculograms and late exercise studies. During long-term follow-up (1 to 4 years) resting radionuclide ventriculography demonstrated a significant improvement in right ventricular ejection fraction (30 +/- 7% to 43 +/- 8%; p less than .001) and right ventricular wall motion index (2.2 +/- 0.4 to 1.5 +/- 0.5; p less than .001) in 18 patients who survived longer than 1 year. Fourteen of these patients underwent upright bicycle exercise while off beta-blocking drugs and peak radionuclide ejection fraction was acquired after anaerobic threshold was achieved. Right ventricular ejection fraction increased significantly from 41 +/- 10% to 47 +/- 12% (p less than .001), as did the left ventricular ejection fraction (55 +/- 15% to 60 +/- 12%; p less than .05). The direction and magnitude of change of the right ventricular ejection fraction correlated significantly with the left ventricular ejection fraction (r = .82, p less than .02). Deviations from this correlation occurred in patients who had a decreased forced expiratory volume in 1 sec and an abnormal ventilatory reserve during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)