EFFICACY OF INTRAVENOUS STREPTOKINASE IN ACUTE MYOCARDIAL INFARCTION: ACUTE AND FOLLOW UP STUDY

1987 ◽  
Author(s):  
R Lochan ◽  
S Tyagi ◽  
B S Yadav ◽  
D K M Rao ◽  
A Bhat ◽  
...  

The efficacy of intravenous streptokinase on recanalization of the 'infarct vessel' and its effect on left ventricular function was assessed in two groups of patients. Group I consisted of 90 consecutive patients (age 32-75 years, mean 56 years) received 500,000 units of intravenous streptokinase (STK) over 30 minutes within 6 hours of onset of acute myocardial infarction (MI). Forty-eight patients had anterior MI and forty-two had inferior MI. The control group consisted of forty survivors of acute MI comparable in age and site of infarction. In Group I, ten patients were administered STK after baseline coronary angiogram demonstrated total occlusion of infarct related coronary artery. In these patients, serial coronary angiogram were done at intervals of 30 minutes after STK infusion upto a period of 3 hours. Recanalization was seen in all cases within 75-135 minutes (average 120 minutes). Seventy-nine of STK group and all of the control group underwent selective coronary arteriography and contrast left ventriculography within 48 to 72 hours of acute MI. Recanalization of infarct related artery was demonstrated in 72 out of 79 patients (91%) in STK group while 8 (20%) in control group had spontaneous recanalization. Left ventricular ejection fraction (LVEF) was higher in STK group (58%) as compared to control group (49%). Among patients with anterior MI, LVEF was significantly better in STK compared to control group (59% Vs. 44%, p > 0.01)while in inferior MI the difference was not significant (63% Vs. 59.4%, p > 0.05) in the two groups. Follow up study in 20 STK patients at 6 months revealed a decrease in residual stenosis from 75 ± 8% to 60 ± 6% and improvement in LVEF from 59 ± 8% to 68 ± 12% (p > 0.01). In conclusion, intravenous STK in acute MI results in high rate of infarct vessel patency and improved global left ventricular function during both early and late follow up period.

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Paul F Teunissen ◽  
Stefan A Timmer ◽  
Ibrahim Danad ◽  
Hans J Harms ◽  
Pieter G Raijmakers ◽  
...  

Introduction: In patients with acute myocardial infarction (AMI), coronary vasomotor function is not only impaired in the myocardial territory supplied by the culprit-artery but also in remote myocardium supplied by angiographically normal vessels. Aims: The aim was to investigate the temporal evolution of coronary vasodilatory reserve in patients with AMI by use of [15O]H2O PET, after successful percutaneous coronary intervention (PCI). Methods: Fourty-four patients with AMI and successful revascularization by PCI were included (i.e. TIMI II or III flow after coronary stenting). Subjects were examined one week and three months after AMI with [15O]H2O PET to assess the coronary flow reserve (CFR). CFR was defined as the ratio of myocardial blood flow during hyperemia (hMBF) and rest (MBF). Additionally, 45 age and sex matched subjects without a prior cardiac history underwent similar scanning procedures and served as a control group. Results: At baseline, CFR averaged 1.77 ± 0.63 in infarcted myocardium versus 2.41 ± 0.79 in remote myocardium (p < 0.001). In comparison, CFR in the control group averaged 4.16 ± 1.45 (p = 0.001 versus both). During follow-up, the CFR increased from 1.77 ± 0.63 to 2.75 ± 0.89 in infarcted myocardium (p < 0.001), and from 2.41 ± 0.79 to 2.85 ± 0.75 in remote myocardium (p = 0.001). This was predominantly due to an increase in hMBF, from 1.64 ± 0.54 to 2.19 ± 0.74 mL/min/g in infarcted myocardium (p < 0.001), and 2.20 ± 0.56 to 2.61 ± 0.65 mL/min/g in remote myocardium (p = 0.001). Conclusions: Coronary vasodilatory reserve is impaired in both ischemic and remote myocardium directly after AMI. Following successful revascularization, the coronary vasodilatory reserve significantly improved in both regions. As a consequence, these early and late post-infarct alterations in remote myocardium may also affect temporal infarct evolution and recovery of left ventricular function.


1988 ◽  
Vol 59 (03) ◽  
pp. 353-356 ◽  
Author(s):  
S Dalby Kristensen ◽  
P C Milner ◽  
J F Martin

SummaryThe bleeding time is shortened and the mean platelet volume is increased in the acute phase of myocardial infarction. In this follow-up study we repeated the measurement of the bleeding time, the platelet count and the platelet volume distribution in 18 patients who had suffered from a definite acute myocardial infarction two years before and in 16 control patients who had been admitted with chest pain but no definite myocardial infarction at that time. At the time of follow-up the bleeding time was significantly lengthened in the myocardial infarction group (median values = 169 s and 209 s respectively), whereas it had shortened in the control group (median values = 258 s and 228 s respectively). Comparison of the platelet volume distribution curves of the myocardial infarction patients at time of infarction and 2 years later revealed a significantly higher percentage of small platelets and significantly lower percentages of both medium-sized and large platelets at the time of infarction. These changes in the platelet volume distribution could indicate consumption of medium-sized and large platelets at the time of myocardial infarction. None of the measured variables predicted which of the patients with acute myocardial infarction would subsequently re-infarct or die. In the patients studied with definite ischaemic heart disease (n = 26) a significant negative correlation between bleeding time and mean platelet volume was found. The shortened bleeding time in myocardial infarction is related to the acute event itself or preceeds it, but is reversed two years later.


Author(s):  
Chan Soon Park ◽  
Han-Mo Yang ◽  
You-Jeong Ki ◽  
Jeehoon Kang ◽  
Jung-Kyu Han ◽  
...  

Background: β-Blockers can improve prognosis after acute myocardial infarction. However, it remains unclear how long β-blockers should be prescribed. Methods: We included patients from the prospective, nationwide Korea Acute Myocardial Infarction Registry-National Institutes of Health registry and collected data on β-blockers and left ventricular ejection fraction (LVEF) at 1-year follow-up. Patients were stratified into 2 groups: 1001 patients with a 1-year LVEF<50% and 3007 patients with a 1-year LVEF≥50%. The primary outcome was 2-year all-cause mortality from the 1-year follow-up. Results: A total of 3177 patients received β-blockers at 1 year, and 151 patients died during the 2-year follow-up from 1 year after index hospitalization. β-Blockers showed survival benefits in patients with a 1-year LVEF<50% (log-rank P =0.001) but not in those with a 1-year LVEF≥50% (log-rank P =0.311). After adjusting covariates, β-blockers were associated with a 51% reduction in mortality in patients with a 1-year LVEF<50% ( P =0.020) but not in their counterparts ( P =0.322). Indeed, there was a prognostic interaction between the use of β-blockers at 1 year and 1-year LVEF ( P for interaction=0.004). Conclusions: Use of β-blockers at 1-year follow-up after acute MI was associated with improved outcomes in patients with an LVEF<50% at 1 year but not in those with an LVEF>50% at 1 year. This study provides valuable information about differential responsiveness to β-blockers according to 1-year LVEF and might suggest the proper duration of β-blockers after acute MI. Registration: URL: http://cris.nih.go.kr/cris/en/ ; Unique identifier: KCT0000863.


2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Rafał Wyderka ◽  
Wojciech Wojakowski ◽  
Tomasz Jadczyk ◽  
Katarzyna Maślankiewicz ◽  
Zofia Parma ◽  
...  

Mobilization of stem cells in acute MI might signify the reparatory response.Aim of the Study. Prospective evaluation of correlation between CD34+CXCR4+ cell mobilization and improvement of LVEF and remodeling in patients with acute MI in 1-year followup.Methods. 50 patients with MI, 28 with stable angina (SAP), and 20 individuals with no CAD (CTRL). CD34+CXCR4+ cells, SDF-1, G-CSF, troponin I (TnI) and NT-proBNP were measured on admission and 1 year after MI. Echocardiography and ergospirometry were carried out after 1 year.Results. Number of CD34+CXCR4+ cells in acute MI was significantly higher in comparison with SAP and CTRL, but lower in patients with decreased LVEF ≤40%. In patients who had significant LVEF increase ≥5% in 1 year FU the number of cells in acute MI was significantly higher versus patients with no LVEF improvement. Number of cells was positively correlated () with absolute LVEF change and inversely with absolute change of ESD and EDD in 1-year FU. Mobilization of CD34+CXCR4+ cells in acute MI was negatively correlated with maximum TnI and NT-proBNP levels.Conclusion. Mobilization of CD34+CXCR4+ cells in acute MI shows significant positive correlation with improvement of LVEF after 1 year.


Author(s):  
Yi-Wei Kao ◽  
Ben-Chang Shia ◽  
Huei-Chen Chiang ◽  
Mingchih Chen ◽  
Szu-Yuan Wu

Accumulating evidence has shown a significant correlation between periodontal diseases and systemic diseases. In this study, we investigated the association between the frequency of tooth scaling and acute myocardial infarction (AMI). Here, a group of 7164 participants who underwent tooth scaling was compared with another group of 7164 participants without tooth scaling through propensity score matching to assess AMI risk by Cox’s proportional hazard regression. The results show that the hazard ratio of AMI from the tooth scaling group was 0.543 (0.441, 0.670) and the average expenses of AMI in the follow up period was USD 265.76, while the average expenses of AMI in follow up period for control group was USD 292.47. The tooth scaling group was further divided into two subgroups, namely A and B, to check the influence of tooth scaling frequency on AMI risk. We observed that (1) the incidence rate of AMI in the group without any tooth scaling was 3.5%, which is significantly higher than the incidence of 1.9% in the group with tooth scaling; (2) the tooth scaling group had lower total medical expenditures than those of the other group because of the high medical expenditure associated with AMI; and (3) participants who underwent tooth scaling had a lower AMI risk than those who never underwent tooth scaling had. Therefore, the results of this study demonstrate the importance of preventive medicine.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Florian Leuschner ◽  
Jin Li ◽  
Stefan Göser ◽  
Lars Reinhardt ◽  
Renate Öttl ◽  
...  

Application of antibodies against cardiac troponin I (cTnI-Ab) can induce dilation and dysfunction of the heart in mice. Recently, we demonstrated that immunization with cTnI induces inflammation and fibrosis in myocardium of mice. Others have shown that autoanti-bodies to cTnI are present in patients with acute coronary syndrome. But little is known about the clinical relevance of detected cTnI-Ab. First, anti-cTnI and anti-cTnT antibody titers were measured in sera from 272 patients with dilated- (DCM) and 185 with ischemic- (ICM) cardiomyopathy. Secondly, 108 patients with acute myocardial infarction (AMI) were included for a follow-up study. Heart characteristics were determined by magnetic resonance imaging 4 days and 6 –9 months after AMI. Altogether, in 7,0% of patients with DCM and in 9,2% with ICM an anti-cTnI IgG antibody titer ≥1:160 was measured. In contrast, only in 1,7% of patients with DCM and in 0,5% with ICM an anti-cTnT IgG antibody titer ≥1:160 was detected. Ten out of 108 patients included in the follow-up study were tested positive for cTnI-Ab with IgG Ab titers ≥1:160. TnI-Ab negative patients showed a significant increase in LVEF and stroke volume 6 –9 months after AMI. In contrast, there was no significant increase in LVEF and stroke volume in TnI-Ab positive patients. We demonstrate for the first time that the prevalence of cTnI-Abs in patients with AMI has an impact on the improvement of the LVEF over a study period of 6 –9 months.


2018 ◽  
Vol 20 (4) ◽  
pp. 396-406 ◽  
Author(s):  
Toshiyuki Kimura ◽  
Véronique L Roger ◽  
Nozomi Watanabe ◽  
Sergio Barros-Gomes ◽  
Yan Topilsky ◽  
...  

Abstract Aims Mechanisms of chronic ischaemic mitral regurgitation (IMR) are well-characterized by apically tethered leaflet caused by papillary muscles (PMs) displacement and adynamic mitral apparatus. We investigated the unique geometry and dynamics of the mitral apparatus in first acute myocardial infarction (MI) by using quantified 3D echocardiography. Methods and results We prospectively performed 3D echocardiography 2.3 ± 1.8 days after first MI, in 174 matched patients with (n = 87) and without IMR (n = 87). 3D echocardiography of left ventricular (LV) volumes and of mitral apparatus dynamics throughout cardiac cycle was quantified. Similar mitral quantification was obtained at chronic post-MI stage (n = 44). Mechanistically, acute IMR was associated with larger and flatter annulus (area 9.29 ± 1.74 cm2 vs. 8.57 ± 1.94 cm2, P = 0.002, saddle shape 12.7 ± 4.5% vs. 15.0 ± 4.6%, P = 0.001), and larger tenting (length 6.36 ± 1.78 mm vs. 5.60 ± 1.55 mm, P = 0.003) but vs. chronic MI, mitral apparatus displayed smaller alterations (all P < 0.01) and annular size, PM movement remained dynamic (all P < 0.01). Specific to acute IMR, without PM apical displacement (P > 0.70), greater separation (21.7 ± 4.9 mm vs. 20.0 ± 3.4 mm, P = 0.01), and widest angulation of PM (38.4 ± 6.2° for moderate vs. 33.5 ± 7.3° for mild vs. 31.4 ± 6.3° for no-IMR, P = 0.0009) wider vs. chronic MI (P < 0.01). Conclusions 3D echocardiography of patients with first MI provides insights into unique 4D dynamics of the mitral apparatus in acute IMR. Mitral apparatus remained dynamic in acute MI and distinct IMR mechanism in acute MI is not PM displacement seen in chronic IMR but separation and excess angulation of PM deforming the mitral valve, probably because of sudden-onset regional wall motion abnormality without apparent global LV remodelling. This specific mechanism should be considered in novel therapeutic strategies for IMR complicating acute MI.


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