Obstructive sleep apnoea inhibits the recovery of left ventricular function in patients with acute myocardial infarction.

AIMS: It has been suggested that obstructive sleep apnoea syndrome (OSA) may be a direct cause of left ventricular (LV) systolic dysfunction. This study was designed to examine our hypothesis that OSA inhibits the recovery of LV function in patients with acute myocardial infarction (AMI). METHODS AND RESULTS: Our 86 consecutive first-AMI patients underwent primary percutaneous coronary intervention (PCI). All patients underwent polysomnography and OSA was defined as an apnoea-hypoapnoea index (AHI) > or =15 events/h, of which more than 50% were obstructive. Left ventriculograms immediately after PCI and at 21 days were used to evaluate LV ejection fraction (LVEF), LV end-diastolic volume index, and regional wall motion (RWM) within the infarct area. OSA was observed in 37 patients (43%). All three indices of LV function after primary PCI were comparable between the two groups. Increases in LVEF and RWM during admission were significantly lower in OSA patients than those without OSA (delta LVEF: -0.3+/-9.6 vs. 7.4+/-7.2%, P < 0.001; delta RWM: 0.26+/-1.04 SD/chord vs. 1.16+/-1.20 SD/chord, P = 0.002). Multiple regression analysis showed that AHI correlated negatively with delta LVEF and delta RWM. CONCLUSION: The novel finding is that OSA may inhibit the recovery of LV function in patients with AMI.     

Evaluation of transmural myocardial perfusion by ultra-harmonic myocardial contrast echocardiography in reperfused acute myocardial infarction.

BACKGROUND: The transmural distribution of myocardial perfusion is important for predicting the contractile reverse of an infarcted wall in reperfused acute myocardial infarction (AMI). Evaluating transmural myocardial perfusion by myocardial contrast echocardiography (MCE) could predict the long-term recovery of left ventricular (LV) function. METHODS AND RESULTS: The study group comprised 20 consecutive patients with a first-episode anterior AMI with total occlusion of the proximal left anterior descending artery, who underwent successful percutaneous coronary intervention within 24 h of onset. MCE was performed on the 15th day after the onset, using ultraharmonic gray-scale imaging with intermittent end-systolic triggering every 4 beats or every 6 beats. Regions of interest were placed over both the endocardial and epicardial region at the mid-septal level. Regional wall motion (RWM) of the infarcted anterior wall and global LV function were assessed by 2-dimensional echocardiography and left ventriculography in both the acute and chronic phase. The transmural distribution of myocardial perfusion by MCE demonstrated a significant relation with RWM score index (r = 0.75, p = 0.0004). Recovery of RWM and LV ejection fraction (LVEF) at 6 months after reperfusion was significantly greater in the group with good perfusion of the epicardium according to MCE than in the poor perfusion group [RWM (SD/cord); -1.23+/-0.91 vs -3.51+/-0.84, p = 0.001, LVEF (%); 63.8+/-10.4 vs 47.0+/-3.4, p = 0.04]. CONCLUSIONS: Assessing the transmural distribution of myocardial perfusion by MCE can predict the long-term recovery of LV function after a reperfused AMI.     

Relationship between terminal QRS distortion on the admission electrocardiogram and the time course of left ventricular wall motion in anterior wall acute myocardial infarction

In order to clarify the time course of left ventricular (LV) wall motion in patients with anterior acute myocardial infarction (AMI) showing terminal QRS distortion on the admission electrocardiogram (ECG), the present study examined 106 patients with their first anterior AMI (< or =6 h) who underwent emergency coronary arteriography and cardiac cathetherization at 1 and 6 months after the infarction. The patients were classified into 2 groups according to the presence (group A, n=23) or absence (group B, n=83) of terminal QRS distortion (emergence of the J point at > or =50% of the R-wave amplitude in leads with QR configuration and/or absence of S waves in leads with RS configuration) on the admission ECG. Group A had a lower LV ejection fraction and more reduced regional wall motion (RWM) in the infarct region at both 1 and 6 months after AMI than group B. The degree of improvement in RWM between 1 and 6 months after AMI was less in group A than in group B (-0.1+/-0.5 vs 0.4+/-0.6 SD/chord, p<0.01). This study indicates that patients with anterior AMI showing terminal QRS distortion on the admission ECG have more severely depressed LV wall motion and less improvement in RWM in the infarct region in the healing stage, suggesting that this sign is an indicator of severe myocardial damage.     

Coronary flow velocity reserve in hypertensive patients with left ventricular systolic dysfunction

BACKGROUND: Hypertensive microvascular disease is speculated to be a limiting factor for the ability of left ventricular (LV) hypertrophy to maintain LV systolic function in systemic hypertension. The role of coronary reserve, which may be affected by microvascular disease, remains uncertain in the pathophysiology of hypertensive heart disease. HYPOTHESIS: A progressive impairment of coronary flow velocity reserve (CFVR) according to the presence and severity of LV systolic dysfunction is anticipated to occur in hypertension. METHODS: According to the absence or presence of LV dysfunction (LV fractional shortening - FS% < 30), two groups of hypertensive patients were investigated: HP1 (n = 9, FS% = 36+/-6) and HP2 (n = 13, FS% = 18+/-6). Eight normal subjects (NL) served as controls (LVFS% = 35+/-3). Doppler blood flow velocity was obtained from the left anterior descending coronary artery using transesophageal echocardiography before, and during 6-min continuous adenosine infusion (140 microg x kg(-1) x min(-1) intravenous). The CFVR was calculated as the ratio of maximal to baseline peak diastolic flow velocities. RESULTS: The comparison among NL, HP1, and HP2 groups showed statistically different (p < 0.05) mass index (101+/-18, 172+/-46, and 257+/-54 g x m(-2)), end-systolic wall stress (76.9+/-14.4, 78.4+/-23.9, and 174.5+/-43.0 10(3) x dyn x cm(-2)), and CFVR (3.5+/-0.6, 3.2+/-0.4, and 2.6+/-0.8), respectively. The CFVR correlated significantly and directly with LVFS% (r = 0.40) and correlated inversely with both mass index (r = -0.54) and end-systolic stress (r = -0.40). CONCLUSIONS: These results indicate that CFVR impairment is weakly related to LV dysfunction in hypertension.     

Effects of reperfusion on left ventricular ejection fraction and volume after acute myocardial infarction.

The effects of reperfusion on left ventricular (LV) function and volume were studied in patients with evolving acute myocardial infarction (AMI). We analyzed the LV ejection fraction and volume in patients who had been admitted within 24 h of the onset of their first AMI with culprit lesion of #6, #7 and #1 (American Heart Association classification). Sixty-five patients (Re group) received successful reperfusion therapy within 6 h after the AMI. The other 60 patients (Oc group), who were admitted from 6 to 24 h after the AMI, received conservative therapy. Patients with re-obstruction of the culprit lesion after reperfusion therapy were excluded from the Re group. Patients with spontaneous recanalization following conservative therapy were excluded from the Oc group. The LV ejection fraction (LVEF), LV end-systolic volume index (LVESVI), and LV end-diastolic volume index (LVEDVI) were measured using a modified Dodge's formula by left ventriculography performed 4 weeks after the AMI. LVEF in the Re group was significantly greater than in the Oc group (57 +/- 12 vs 49 +/- 11%) (mean +/- SD, p less than 0.01). LVESVI in the Re group was significantly smaller than in the Oc group (30 +/- 13 vs 38 +/- 16 ml/m2, p less than 0.01). Although LVEDVI was not significantly different between the 2 groups, in patients with a responsible coronary lesion of segment #6, LVEDVI in the Re group was significantly smaller than in the Oc group (67 +/- 14 vs 77 +/- 18 ml/m2, p less than 0.05). Although LVEF and LV volume correlated in both groups, the correlation was weak (r = 0.40-0.42), suggesting that LV volume was not dependent solely on LV functional recovery. The incidence of ventricular aneurysm in the Re group was significantly lower than in the Oc group (15.4 vs 45.0%, p less than 0.01). Multivariate analysis selected reperfusion of the responsible coronary artery as one of the factors significantly associated with a reduction of LVEDVI, LVESVI, an improvement of LVEF, and a decrease in the rate of aneurysm formation. In summary, our results indicated that reperfusion improved EF, reduced LV volume, and decreased the rate of aneurysm formation as compared to non-reperfusion, which suggests that reperfusion therapy is beneficial for both functional recovery and ventricular remodeling.     

Pressure-derived collateral flow index as a parameter of microvascular dysfunction in acute myocardial infarction.

OBJECTIVES: The goal of this study was to examine the implications of the pressure-derived collateral flow index (CFIp) in acute myocardial infarction (AMI). BACKGROUND: Higher CFIp is associated with less severe myocardial ischemia during angioplasty in the non-infarcted heart. It remains unknown whether CFIp also identifies collateral function in AMI patients with and without no-reflow phenomenon. METHODS: The study population included 48 patients with a first AMI. After successful percutaneous transluminal coronary angioplasty (PTCA) stent, we measured mean aortic pressure (Pa), central venous pressure (Pv) and coronary wedge pressure (Pcw) of the infarct-related artery to calculate: CFIp = (Pcw - Pv)/(Pa - Pv). Myocardial contrast echocardiography (MCE) was performed with the intracoronary injection of microbubbles to assess myocardial perfusion. Left ventriculograms at days 1 and 28 were provided for the measurement of the regional wall motion (RWM, SD/chord). RESULTS: There was no difference in CFIp among subsets based on angiographic collateral grades (grade 0, 1, 2, 3; 0.28 +/- 0.07, 0.27 +/- 0.09, 0.27 +/- 0.08, 0.23 +/- 0.08, p = NS). The CFIp was significantly higher in patients with MCE no-reflow (n = 16) than in those with MCE reflow (n = 32) (0.34 +/- 0.07 vs. 0.23 +/- 0.06, p < 0.01). There was a significant inverse correlation between the extent of functional improvement (DeltaRWM[28 d-1 d]) and CFIp (r = 0.56, p < 0.01), implying that higher CFIp is associated with worse functional improvement. CONCLUSIONS: In AMI, CFIp is unlikely to reflect collateral function but seems to increase with the severity of microvascular dysfunction. Because higher CFIp was associated with poorer functional recovery, it provides a simple and useful estimate of clinical outcomes in AMI.     

Prediction of remote left ventricular volumes and functions after acute myocardial infarction with successful coronary intervention.

BACKGROUND: The scintigraphic perfusion defect size (DS) at 1 week after acute myocardial infarction (AMI) predicts remote left ventricular (LV) volumes and LV ejection fraction (LVEF). The present study examined whether LV volumes and LVEF 6 months after AMI may be better predicted by the combination of LV volumes and LVEF just after reperfusion, and DS at 1 week, after AMI in patients with Thrombolysis In Myocardial Infarction (TIMI) grade III reperfusion by percutaneous coronary intervention. METHODS AND RESULTS: In 48 patients with AMI and TIMI grade III reperfusion, quantitative gated SPECT (QGS) was performed just after reperfusion, and at 1 week and 6 months after AMI. LV end-diastolic volume index decreased (108+/-8 to 93+/-6 ml/m(2), p<0.05) and LVEF increased (44+/-3 to 50+/-2%, p<0.05) 6 months after AMI. In addition, they were better predicted by a combination of LV volumes and LVEF just after reperfusion and DS at 1 week after AMI. CONCLUSIONS: In AMI with TIMI grade III reperfusion, LV volumes and LVEF at 6 months after MI correlate with the values obtained just after reperfusion. Myocardial perfusion imaging combined with QGS at reperfusion may predict these late-phase parameters.     

Relation of left ventricular dilation during acute myocardial infarction to systolic performance, diastolic dysfunction, infarct size and location

The quantification of left ventricular (LV) volumes and assessment of their relation to systolic and diastolic dysfunction, infarct size and anatomic location were performed in 54 patients with a first acute myocardial infarction (AMI). Blood pool radionuclide angiography was used to assess LV end-diastolic, end-systolic, and stroke volume indexes, ejection fraction and peak diastolic filling rate. Infarct size was estimated from plasma MB creatine kinase activity. Substantial LV dilation occurred within the initial 24 hours of AMI. The peak diastolic filling rate was low, even in those patients with a normal ejection fraction. In comparison with inferior AMI (n = 25), patients with anterior AMI (n = 29) had a larger end-diastolic volume index (105 +/- 8 vs 81 +/- 4 ml/m2, p less than 0.01) and end-systolic volume index (64 +/- 7 vs 37 +/- 4 ml/m2, p less than 0.001), but similar stroke volume index (41 +/- 3 vs 43 +/- 2 ml/m2, difference not significant). No significant relation was noted between infarct size estimated by MB creatine kinase and any volumetric index. On repeat study (day 10 after AMI), end-diastolic and end-systolic volume indexes increased further (p less than 0.05 vs day 1) but ejection fraction and peak diastolic filling rate were unchanged. It was concluded that: (1) LV dilation occurs within hours of AMI in both inferior and anterior AMI, but is more marked in the latter; (2) significant LV diastolic dysfunction is the rule, even in patients with preserved LV systolic function; and (3) LV dilation is an early compensatory mechanism that maintains normal stroke volume, even in patients with severely reduced LV function.     

Comparison of real-time contrast echocardiography and low-dose dobutamine stress echocardiography in predicting the left ventricular functional recovery in patients after acute myocardial infarction under different therapeutic intervention

BACKGROUND: Early prediction of left ventricular (LV) functional recovery after acute myocardial infarction (AMI) remains challenging. This prospective study aims to compare real-time myocardial contrast echocardiography (MCE) with low-dose dobutamine stress echocardiography (LDDSE) in predicting the LV functional recovery in patients after AMI who underwent different therapeutic interventions. METHODS: Ninety-two patients with AMI were divided into 3 groups: primary coronary intervention group (n=34), thrombolysis group (n=30) and conservative therapy group (n=28). MCE was performed 2.3+/-0.7 days after chest pain onset. LDDSE was done within 2 days of MCE study. Follow-up echocardiography was performed 4 months later. RESULTS: Patients treated by primary coronary intervention or thrombolysis had significantly lower regional perfusion score (0.65+/-0.53 vs. 1.01+/-0.49, p=0.008; 0.78+/-0.55 vs. 1.01+/-0.49, p=0.03), better contractile reserve (regional dobutamine Deltawall motion score -1.12+/-0.39 vs. -0.80+/-0.43, p=0.01; -0.99+/-0.50 vs. -0.80+/-0.43, p=0.08) and LV function recovery (regional Deltawall motion score -1.67+/-0.53 vs. -1.02+/-0.46, p=0.003; -1.42+/-0.58 vs. -1.02+/-0.46, p=0.03) than those of conservative therapy group. MCE and LDDSE showed good concordance for predicting LV functional recovery (kappa=0.63, p<0.001). Perfusion score index had a good correlation with LV functional recovery (r=-0.75, p<0.001). CONCLUSIONS: This study demonstrates that perfusion score index obtained from real-time MCE is comparable to LDDSE in predicting the LV functional recovery even under different therapeutic interventions. Revascularization results in better preservation of myocardial microvascular integrity, regional contractile reserve and LV functional recovery.     

Clinical significance of acute-phase endothelin-1 in acute myocardial infarction patients treated with direct coronary angioplasty.

BACKGROUND: The aim of the present study was to investigate the relationship between plasma concentrations of endothelin (ET)-1 and clinical outcome (including mortality) and left ventricular (LV) systolic function in acute myocardial infarction (AMI). METHODS AND RESULTS: The study group comprised 110 consecutive first-AMI patients who were successfully reperfused by primary coronary intervention. Plasma ET-1 concentrations were evaluated 24 h from onset and the patients were divided into 2 groups according to the median value, either a high group (H group: > or = 2.90 pg/ml plasma ET-1; n = 55) or low group (L group: < 2.90 pg/ml plasma ET-1; n = 55). Major complications and LV systolic function were monitored in the 2 groups. Both highly sensitive C-reactive protein (hs-CRP) and brain natriuretic peptide (BNP) showed a significant positive correlation with ET-1 (BNP: r = 048, p < 0.0001, hs-CRP: r = 0.43, p < 0.001). Chronic stage left ventricular ejection fraction (LVEF) and left ventricular end-diastolic volume index (LVEDVI) were significantly poorer in the H group (LVEF: 51+/-15% vs 60+/-13%, p = 0.003, LVEDVI: 74+/-19 ml/m2 vs 66+/-14 ml/m2, p < 0.05). There were significantly more major complications in the H group than in the L group (cardiogenic shock: 18% vs 5%, p = 0.04; cardiac death: 13% vs 0%, p < 0.01). CONCLUSIONS: In the setting of AMI, plasma ET-1 concentrations may be closely related to LV systolic dysfunction and poor patient outcome, including mortality.     

Determinants of Left Ventricular Functional Recovery After Thrombolytic Therapy and/or Immediate Coronary Angioplasty in Acute Myocardial Infarction

To determine the effect of thrombolytic therapy and/or immediate coronary angioplasty (PTCA) on left ventricular function, 129 patients with acute transmural myocardial infarction were retrospectively studied. Treatment strategies included thrombolytic therapy alone (n = 29), PTCA alone (n = 41), and combined thrombolytic therapy and PTCA (n = 59). Left ventricular ejection fraction (LVEF) and infarct zone regional wall motion (RWM) were determined from contrast ventriculography obtained acutely and at day 7–10. In the overall group, there was a 2 ± 9% increase in LVEF (p < 0.02) and a 0.7 ± 1.2 SD/chord increase in RWM (p < 0.0001) between day 1 and day J-10. Patients with a patent infarct vessel at day 7–10 had a more significant change (Δ) in LVEF (3 ± 8 vs ?5 ± 9%, p = 0.0002) and RWM (0.8 ± 1.2 vs 0.1 ± 1.0 SD/chord, p < 0.02) than patients with an occluded vessel. Patients with a residual stenosis < 70% at day 7–10 manifested a greater ΔLVEF (3 ± 8vs-5 ± 9%, p < 0.01) and ΔRWN (0.9 ± 1.2 vs 0.1 ± 1.0 SD/ chord, p < 0.05) than patients who were occluded. There was a negative correlation between residual stenosis and ΔRWM (p < 0.04). Patients treated < 3 hours after symptom onset demonstrated a more significant ΔRWM when compared to patients treated ≥ 3 hours (1.0 ± 1.3 vs 0.5 ± 1.1 SD/chord, p < 0.04). Patients treated with combined thrombolytic therapy and PTCA were observed to have a greater ARWM than patients treated with thrombolytic therapy alone (0.8 ± 1.2 vs 0.2 ±0.9 SD/chord, p < 0.05). Patients with an LVEF > 40% demonstrated a more significant ΔLVEF than patients; ± 40% (7 ± 8vs 1 ± 8%, p < 0.007). A significant improvement in ΔLVEF was noted only in patients with an anterior infarction when compared to patients with an inferior infarction. Age, sex, presence of multivessel disease, history of prior myocardial infarction, initial patency of the infarct vessel, and presence of collaterals had no effect on left ventricular function. Stepwise multiple regression identified residual stenosis, time to treatment, and the degree of initial global impairment as the major joint predictors of ventricular functional recovery. (J Interven Cardiol 1988:1:3)     

Effects of left ventricular unloading by Impella recover LP2.5 on coronary hemodynamics.

OBJECTIVES: We studied the effects of LV unloading by the Impella on coronary hemodynamics by simultaneously measuring intracoronary pressure and flow and the derived parameters fractional flow reserve (FFR), coronary flow velocity reserve (CFVR), and coronary microvascular resistance (MR). BACKGROUND: Patients with compromised left ventricular (LV) function undergoing high-risk percutaneous coronary intervention (PCI) may benefit from LV unloading. Limited information is available on the effects of LV unloading on coronary hemodynamics. METHODS: Eleven patients (mean LV ejection fraction of 35 +/- 11%) underwent PCI during LV support by the LV unloading device (Impella Recover LP2.5). Intracoronary measurements were performed in a nonstenotic coronary artery after the PCI, before and after adenosine-induced hyperemia at four different support levels (0-2.5 L/min). RESULTS: Aortic and coronary pressure increased with increasing support levels, whereas FFR remained unchanged. Baseline flow velocity remained unchanged, while hyperemic flow velocity and CFVR increased significantly with increasing support levels (61 +/- 24 to 72 +/- 27 cm/sec, P = 0.001 and 1.88 +/- 0.52 to 2.34 +/- 0.63, P < 0.001 respectively). The difference between baseline MR and hyperemic MR significantly increased with increasing support levels (1.28 +/- 1.32 to 1.89 +/- 1.43 mm Hg cm(-1) sec, P = 0.005). CONCLUSIONS: Unloading of the LV by the Impella increased aortic and intracoronary pressure, hyperemic flow velocity and CFVR, and decreased MR. The Impella-induced increase in coronary flow, probably results from both an increased perfusion pressure and a decreased LV volume-related intramyocardial resistance.     

Effect of intraaortic balloon pumping on left ventricular function in patients with persistent ST segment elevation after revascularization for acute myocardial infarction.

The purpose of the present study was to assess the impact of intraaortic balloon pumping (IABP) in patients with persistent ST elevation who underwent revascularization within 6 h of their first acute anterior myocardial infarction (AMI). Persistent ST elevation after revascularization was defined as being > or =50% of the initial value on return to the coronary care unit. Twenty-four patients were treated without IABP (control group) and 27 patients were treated with IABP (IABP group). There was no significant difference between the 2 groups in pretreatment left ventricular ejection fraction (LVEF), end-diastolic volume index or end-systolic volume index. After 137+/-46 days, the change in the LVEF was significantly higher in the IABP group than in the control group (5+/-13% vs 13+/-15%, p=0.04). However, the left ventricular end-diastolic volume index was similar between the 2 groups during follow-up (pretreatment: 77+/-19 ml/m(2) vs 74+/-13 ml/m(2), p=0.54; follow-up: 86+/-22 ml/m(2) vs 83+/-18 ml/m(2), p=0.60). These data suggest that IABP enhances the improvement in LVEF independent of remodeling in AMI patients with persistent ST elevation after revascularization.     

Intravenous atrial natriuretic peptide prevents left ventricular remodeling in patients with first anterior acute myocardial infarction

OBJECTIVES: The study evaluates the effect of atrial natriuretic peptide (ANP) compared with nitroglycerin (GTN) on left ventricular (LV) remodeling after first anterior acute myocardial infarction (AMI). BACKGROUND: Compared with GTN, ANP suppresses the renin-angiotensin-aldosterone system and endothelin-1 (ET-1), which stimulate LV remodeling. METHODS: Sixty patients with a first anterior AMI were randomly divided into the ANP (n = 30) or GTN (n = 30) groups after direct percutaneous transluminal coronary angioplasty. We evaluated LV ejection fraction (LVEF), end-diastolic volume index (LVEDVI) and end-systolic volume index (LVESVI) at the acute phase and after one month. We also measured neurohumoral factors during study drug infusion. RESULTS: There was no difference in the baseline characteristics or LVEF (46.9+/-1.0 vs. 46.8+/-1.3%) between the two groups. Although there was no difference in hemodynamics during the infusion periods, the LVEF was significantly improved after one month compared with the baseline value in both groups, but it was improved more in the ANP group than in the GTN group (54.6+/-1.1%, 50.8+/-1.3%, p < 0.05). Left ventricular enlargement was prevented in the ANP group (LVEDVI, 85.8+/-3.1 ml/m2 to 87.3+/-2.7 ml/m2; p = ns, LVESVI, 45.6+/-1.8 ml/m2 to 41.0+/-2.1 ml/m2, p < 0.05) but not in the GTN group (LVEDVI, 86.2+/-4.1 to 100.2+/-3.7, p < 0.01; LVESVI, 46.3+/-2.8 ml/m2 to 51.1+/-3.0 ml/m2, p = ns). During the infusion, ANP suppressed plasma levels of aldosterone, angiotensin II and ET-1 compared with GTN. CONCLUSIONS: These findings indicate that in patients with a first anterior AMI, an ANP infusion can prevent LV remodeling better than can GTN, and effectively suppresses aldosterone, angiotensin II and ET-1.     

Effects of intravenous atrial natriuretic peptide on cardiac sympathetic nerve activity and left ventricular remodeling in patients with first anterior acute myocardial infarction.

OBJECTIVES: We sought to evaluate the effects of atrial natriuretic peptide (ANP) on cardiac sympathetic nerve activity (CSNA) and left ventricular (LV) remodeling in patients with first anterior acute myocardial infarction (AMI) after primary coronary angioplasty. BACKGROUND: The activation of the renin-angiotensin-aldosterone system (RAAS) prevents the uptake of norepinephrine in the myocardium. Atrial natriuretic peptide, a circulating hormone of cardiac origin, has vasodilatory and diuretic properties, and can inhibit the RAAS. METHODS: We studied 50 patients with first anterior AMI who were randomly assigned to receive ANP (group A) or isosorbide dinitrate (group B) before and after primary coronary angioplasty. The ANP or ISDN was continuously infused >48 h. The extent score (ES) was determined from 99mTc-pyrophosphate scintigraphy to evaluate the area of initial myocardial damage 3 to 5 days after primary angioplasty. The LV end-diastolic volume (LVEDV) and LV ejection fraction (LVEF) were determined by left ventriculography 2 weeks later. The delayed heart/mediastinum count (H/M) ratio, delayed total defect score (TDS), and washout rate (WR) were determined from 123I-meta-iodobenzylguanidine scintigraphy after 3 weeks. RESULTS: After primary angioplasty, age, gender, risk factors, peak serum creatine phosphokinase concentration, recanalization time, and ES were similar in the 2 groups. However, in group A (n = 25), the TDS was significantly lower (34 +/- 8 vs. 41 +/- 8; p < 0.05), the H/M ratio was significantly higher (1.96 +/- 0.18 vs. 1.74 +/- 0.23; p < 0.05), and the WR was significantly lower (35 +/- 8% vs. 44 +/- 12%; p < 0.005) than in group B (n = 25). Moreover, the LVEDV and LVEF in group A were better than in group B (LVEDV: 85.5 +/- 28.5 ml vs. 106.3 +/- 39.4 ml [p < 0.05]; LVEF: 47.9 +/- 10.2% vs. 41.5 +/- 11.8% [p < 0.05]). CONCLUSIONS: Intravenous ANP improves CSNA and prevents LV remodeling in patients with first anterior AMI.     

The relationship between acute phase serum amyloid A (SAA) protein concentrations and left ventricular systolic function in acute myocardial infarction patients treated with primary coronary angioplasty

BACKGROUND: Our study was planned to investigate the relationship between plasma levels of serum amyloid A protein (SAA) concentrations and the subsequent left ventricular systolic function in patients with acute myocardial infarction (AMI) treated with primary coronary angioplasty. METHODS AND RESULTS: Reperfusion by primary percutaneous coronary intervention was successful in 486 consecutive AMI patients who were admitted within 12 hours of onset. Plasma SAA concentrations were evaluated 24 hours after onset. Left ventricular (LV) function was serially determined by left ventriculography performed in the acute (soon after recanalization) and chronic phases (6 months after onset). (I) There was no significant correlation between SAA concentration and acute phase left ventricular ejection fraction (LVEF) or regional wall motion (RWM). (II) The SAA concentration was significantly correlated with both highly sensitive C-reactive protein (hs-CRP) and the peak-CK value (hs-CRP: r = 0.69, P < 0.0001, peak-CK: r = 0.21, P = 0.0003). (III) SAA was significantly negatively correlated with both LVEF and RWM in the chronic phase (LVEF: r = -0.42, P = 0.001; RWM: r = -0.41, P = 0.007). (IV) The plasma level of SAA also showed a significant negative correlation with the differences in LVEF between the 2 stages (delta-LVEF) (r = -0.43, P = 0.02). CONCLUSION: In the setting of AMI, plasma SAA concentrations may be closely related to subsequent left-ventricular systolic dysfunction.     

Impact of prodromal angina pectoris and white blood cell count on outcome of patients with acute myocardial infarction

BACKGROUND: Elevation of white blood cell (WBC) count at admission is associated with adverse outcome after acute myocardial infarction (AMI). Prodromal angina, by the mechanism of ischemic preconditioning, improves left ventricular (LV) function and survival after reperfusion therapy in patients with AMI. Recent experimental studies have reported that preconditioning has anti-inflammatory effect. METHODS: This study consisted of 598 patients with first anterior wall AMI who underwent coronary angiography within 12 h after symptom onset. WBC count was measured at the time of hospital admission. Prodromal angina was defined as angina occurring within 24 h before the onset of AMI. Serial measurements of LV ejection fraction (EF) were obtained before reperfusion therapy and before discharge in 421 patients (71%). RESULTS: High WBC count (>10.2 x 103/mm3, n=297) was associated with higher 30-day mortality (8% vs. 4%, p=0.02) and lower predischarge LVEF (51+/-15% vs. 57+/-14%, p<0.001), although there was no significant difference in acute LVEF (47+/-10% vs. 49+/-11%, p=0.07). High WBC count was an independent predictor of 30-day mortality (p=0.009) and predischarge LVEF (p=0.002). Prodromal angina was associated with lower 30-day mortality (3% vs. 7%, p=0.02) and preserved predischarge LVEF (57+/-15% vs. 53+/-14%, p=0.006). Patients with prodromal angina had lower WBC count (10.0+/-3.3 x 10(3)/mm3 vs. 11.0+/-3.9 x 10(3)/mm3, p=0.001) and prodromal angina was an independent predictor of WBC count (p<0.001). CONCLUSIONS: Elevation of WBC count and lack of prodromal angina were associated with impaired LV function and mortality after reperfusion in patients with AMI. Prodromal angina might have contributed to favorable outcome after AMI through its anti-inflammatory effect.     

Persistent ST-segment elevation after primary stenting for acute myocardial infarction: its relation to left ventricular recovery

BACKGROUND: Early restoration of coronary artery patency in acute myocardial infarction (AMI) has been linked to improvement in survival. However, early recanalization of an occluded epicardial coronary artery by either thrombolytic agents or percutaneous transluminal coronary angioplasty (PTCA) does not necessarily lead to left ventricular (LV) function recovery. HYPOTHESIS: The aim of this study was to evaluate the relation between persistent ST elevation shortly after primary stenting for acute myocardial infarction (AMI) and LV recovery. METHODS: Thirty-one patients with primary stenting for AMI were prospectively enrolled. To evaluate the extent of microvascular injury, serial ST-segment analysis on a 12-lead electrocardiogram recording just before and at the end of the coronary intervention was performed. Persistent ST-segment elevation (Persistent Group, n = 11) was defined as > or = 50% of peak ST elevation and resolution (Resolution Group, n = 20) was defined as < 50% of peak ST elevation. Echocardiography was performed on Day 1 and 3 months after primary stenting. RESULTS: At 3 months, infarct zone wall-motion score index (WMSI, 2.1 +/- 0.6 vs. 2.7 +/- 0.3, p < 0.05) was smaller in the Resolution Group than in the Persistent Group, whereas wall motion recovery index (RI, 0.4 +/- 0.3 vs. 0.1 +/- 0.2, p < 0.05) and ejection fraction (58 +/- 5 vs. 43 +/- 10%, p < 0.05) were larger in the Resolution Group than in the Persistent Group. The extent of persistent ST elevation (% ST) shortly after successful recanalization of the infarct-related artery was significantly related to RI at 3 months (r = -0.4, p < 0.05). However, time to reperfusion was not related to RI at 3 months. There was also significant correlation between corrected TIMI frame count and %ST (r = 0.4, p < 0.05). CONCLUSIONS: Persistent ST-segment elevation shortly after successful recanalization (> or = 50% of the peak value), as a marker of impaired microvascular reperfusion, predicts poor LV recovery 3 months after primary stenting for AMI.     

Coronary flow velocity immediately after primary coronary stenting as a predictor of ventricular wall motion recovery in acute myocardial infarction

OBJECTIVES

The purpose of this study was to examine the relationship between the pattern of coronary blood flow velocity immediately after successful primary stenting and the recovery of left ventricular (LV) wall motion in patients with acute myocardial infarction (AMI).

BACKGROUND

It is difficult to predict the recovery of LV wall motion immediately after direct angioplasty in AMI. Recent reports indicate that dysfunctional coronary microcirculation is an important determinant of prognosis for AMI patients after successful reperfusion.

METHODS

We measured left anterior descending coronary flow velocity variables using a Doppler guide wire immediately after successful primary stenting in 31 patients with their first anterior AMI. The patients were divided into two groups: those with and those without early systolic reverse flow (ESRF). Changes in LV regional wall motion (RWM) and ejection fraction (EF) at admission and at discharge were compared between the two groups. Coronary flow velocity variables immediately after primary stenting were compared with changes in left ventriculographic indexes.

RESULTS

The change in RWM was significantly greater in the non-ESRF group than it was in the ESRF group (0.9 ± 0.7 vs. −0.1 ± 0.3 standard deviation/chord, respectively, p < 0.001). The change in EF was also significantly greater in the non-ESRF group than it was in the ESRF group (10 ± 10 vs. 1 ± 6%, respectively, p < 0.05). In the non-ESRF group (diastolic to systolic velocity ratio [DSVR] <3.0), the DSVR correlated positively with the change in RWM (r = 0.60, p < 0.005, n = 24) and the change in EF (r = 0.52, p < 0.01).

CONCLUSIONS

The coronary flow velocity pattern measured immediately after successful primary stenting is predictive of the recovery of regional and global LV function in patients with AMI.     

Plasma matrix metalloproteinase-9 and left ventricular remodelling after acute myocardial infarction in man: a prospective cohort study.

AIM: To describe temporal profiles of plasma matrix metalloproteinases (MMP-2 and MMP-9), and their relationship with echocardiographic (Echo) parameters of left ventricular (LV) function and remodelling, after acute myocardial infarction (AMI) in man. METHODS AND RESULTS: Plasma MMP-2 and MMP-9 were assayed at intervals (0-12, 12-24, 24-48, 48-72, 72-96, and > 96 h) in 91 patients with AMI (ST-elevation/non-ST-elevation 77/24; 73% male; 40% anterior site) and on a single occasion in 172 age- and sex-matched control subjects with stable coronary artery disease. Echo assessment of LV volumes, LV ejection fraction (LVEF), and wall motion index score were assessed before discharge and at follow-up (median 176, range 138-262 days) for patients and on a single occassion in controls. Plasma MMP-2 was similar at all times after AMI, elevated when compared with control (P = 0.005-0.001) and unrelated to LV function or volume during index admission or at follow-up. Maximal MMP-9 was seen at 0-12 h and was elevated when compared with control (P = 0.002) followed by fall to a plateau. Both maximal and plateau MMP-9 concentration correlated with white blood cell (WBC, P = 0.023 to < 0.001) and neutrophil count (P = 0.014 to < 0.001). Maximal MMP-9 had independent predictive value for lower LVEF (P = 0.004) during admission and for greater change in LV end-diastolic volume between admission and follow-up (R = 0.3, P = 0.016). In contrast, higher plateau levels of MMP-9 were associated with relative preservation of LV function (increasing LVEF, P = 0.002; decreasing WMIS, P = 0.009) and less change in end-systolic volume and end-diastolic volumes after discharge (P = 0.001 and 0.024, respectively). CONCLUSION: Both MMP-9 and MMP-2 are elevated following AMI. The biphasic profile of plasma MMP-9 is related to LV remodelling and function following AMI in man. Higher early levels of MMP-9 associate with the extent of LV remodelling and circulating WBC levels. In contrast, higher plateau levels later after AMI are associated with relative preservation of LV function. Temporal profile, rather than absolute magnitude, of MMP-9 activity appears to be important for LV remodelling after AMI.