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PubMed2005

Electromechanical analysis of infarct border zone in chronic myocardial infarction.

To test the hypothesis that alterations in electrical activation sequence contribute to depressed systolic function in the infarct border zone, we examined the anatomic correlation of abnormal electromechanics and infarct geometry in the canine post-myocardial infarction (MI) heart, using a high-resolution MR-based cardiac electromechanical mapping technique. Three to eight weeks after an MI was created in six dogs, a 247-electrode epicardial sock was placed over the ventricular epicardium under thoracotomy. MI location and geometry were evaluated with delayed hyperenhancement MRI. Three-dimensional systolic strains in epicardial and endocardial layers were measured in five short-axis slices with motion-tracking MRI (displacement encoding with stimulated echoes). Epicardial electrical activation was determined from sock recordings immediately before and after the MR scans. The electrodes and MR images were spatially registered to create a total of 160 nodes per heart that contained mechanical, transmural infarct extent, and electrical data. The average depth of the infarct was 55% (SD 11), and the infarct covered 28% (SD 6) of the left ventricular mass. Significantly delayed activation (>mean + 2SD) was observed within the infarct zone. The strain map showed abnormal mechanics, including abnormal stretch and loss of the transmural gradient of radial, circumferential, and longitudinal strains, in the region extending far beyond the infarct zone. We conclude that the border zone is characterized by abnormal mechanics directly coupled with normal electrical depolarization. This indicates that impaired function in the border zone is not contributed by electrical factors but results from mechanical interaction between ischemic and normal myocardium.

Action Potentials↗
PubMed1999

Infarct size is reduced and the frequency of non-Q-wave myocardial infarctions is increased in patients using aspirin at the onset of symptoms.

In an observational study we wanted to investigate whether ongoing use of aspirin in a cohort of 753 patients with acute myocardial infarction was able to (1) reduce infarct size as assessed by peak creatine kinase and lactate dehydrogenase, (2) increase the number of non-Q-wave myocardial infarctions, and (3) to what extent thrombolytic treatment at admission could modify these outcomes. We used an exposed (aspirin+)/nonexposed (aspirin-) cohort design, adjusting for the effects of confounders (age, previous coronary heart disease, current smoking, and the prior use of beta-blockers and long-acting nitrates) as well as for the modifying effect of thrombolytic treatment. Crude and adjusted effects showed that aspirin reduced infarct size only in patients not receiving thrombolytic treatment at admission to hospital (n = 411 patients). In analyzing the occurrence of non-Q-wave versus Q-wave myocardial infarctions, the outcome was dichotomized. Crude odds ratio (OR) for developing a non-Q-wave myocardial infarction in aspirin users was 2. 63 (2p < 0.001), in the restricted cohort of patients receiving thrombolytic treatment, OR was 3.46 (2p = 0.002), whereas in those not receiving such treatment, OR was 1.81 (2p = 0.007). Adjusting for the effects of confounders, retained aspirin was an independent predictor of non-Q-wave myocardial infarctions, an effect that was probably increased (from 51 to 128%) in those who received thrombolytic treatment. Thus, aspirin seems to produce a shift to less severe manifestations of myocardial infarction, an effect that was increased in patients given thrombolytic treatment at admission to hospital.

Aged↗
PubMed1984

Enzymatically and electrocardiographically estimated infarct size in relation to pain in acute myocardial infarction.

In 563 patients with acute myocardial infarction and no previous myocardial infarction, the estimated infarct size was related to the estimated duration of pain and the amount of analgesics given. The size of infarction estimated from analyses of heat-stable lactate dehydrogenase (EC 1.1.1.27) at 12-hour intervals for 48-108 h and from Q- and R-wave changes in the ECG correlated positively, although weakly with duration of the pain and the amount of analgesics given. These data support the hypothesis that larger infarcts, as a group, evolve over a longer time period than smaller infarcts and that the duration of pain in many patients might be an indicator of the infarct size. In the individual patient, however, one cannot predict the size of the infarction from the severity of pain.

Adult↗
PubMed1992

Relationship between serum total cholesterol, infarct size, and early clinical outcome following acute myocardial infarction.

Strategies designed to decrease coronary heart disease (CHD) associated morbidity and mortality have focused primarily on established risk factors, including hypercholesterolemia, systemic hypertension, and cigarette smoking. Indeed, primary and secondary intervention trials have provided evidence for cholesterol lowering as an efficient method of CHD risk reduction. To test the hypothesis that serum total cholesterol influences the clinical outcome following acute myocardial infarction, infarct size, left ventricular ejection fraction, infarct-related vessel patency, and in-hospital cardiac events were determined in 106 consecutive patients given thrombolytic therapy within 5 h of symptom onset. Cumulative 48-hour creatine kinase (CK) release, peak CK, and calculated infarct size did not differ significantly between patients with an admitting serum total cholesterol level less than 200 mg/dl (group 1) and those with a cholesterol level greater than 250 mg/dl (group 2). Total cholesterol did not correlate with either cumulative CK release, peak CK, infarct size, vessel patency, or left ventricular ejection fraction. The vessel patency correlated inversely with cumulative CK release (r = -0.27; p = 0.03) and directly with left ventricular ejection fraction (r = 0.24; p = 0.03). The incidence of in-hospital cardiac events including recurrent infarction, congestive heart failure, and death was 6.9, 13.9, and 2.6%, respectively, and did not differ significantly between patient groups. Thus, although serum total cholesterol has been shown to influence CHD incidence, morbidity, and overall mortality, the findings of our study suggest that it does not impact directly on infarct size, left ventricular function, or in-hospital clinical outcome among patients sustaining acute myocardial infarction.

Cholesterol↗
PubMed1992

A randomized trial of late reperfusion therapy for acute myocardial infarction. Thrombolysis and Angioplasty in Myocardial Infarction-6 Study Group.

BACKGROUND: Experimental and observational clinical studies of acute coronary occlusion have suggested that late reperfusion prevents infarct expansion and facilitates myocardial healing. The purpose of this trial was to assess whether infarct vessel patency could be achieved in late-entry patients and what benefit, if any, can be demonstrated. METHODS AND RESULTS: In a double-blind fashion, 197 patients with 6 to 24 hours of symptoms and ECG ST elevation were randomly assigned to tissue-type plasminogen activator (100 mg over 2 hours) or placebo. Coronary angiography within 24 hours was used to determine infarct vessel patency status. Patients with infarct-related occluded arteries were then eligible for a second randomization to either angioplasty (34 patients) or no angioplasty (37 patients). Ventricular function and cavity size were reassessed at 1 month by gated blood pool scintigraphy and at 6 months by repeat cardiac catheterization. The primary end point, infarct vessel patency, was 65% for plasminogen activator patients compared with 27% in the placebo group (p less than 0.0001). There were no differences between these groups in ejection fraction or infarct zone regional wall motion at 1 or 6 months. At 6 months, infarct vessel patency was 59% in both groups. In the placebo group, there was a significant increase in end-diastolic volume from acute phase of 127 ml to 159 ml at 6-month follow-up (p = 0.006) but no increase in cavity size for the plasminogen activator group patients. Coronary angioplasty was associated with an initial 81% recanalization success and improved ventricular function at 1 month, but by late follow-up no advantage could be demonstrated for this procedure, and there was a 38% spontaneous recanalization rate in the patients assigned to no angioplasty. CONCLUSIONS: The study demonstrates that it is possible to achieve infarct vessel recanalization in the majority of late-entry patients with either thrombolytic therapy or angioplasty. Thrombolytic intervention had a favorable effect on prevention of cavity dilatation and left ventricular remodeling, but there are no late benefits on systolic function after thrombolysis or coronary angioplasty. The conclusions concerning overall potential benefit of applying late reperfusion therapy will require data from large-scale trials designed to assess mortality reduction.

Angioplasty, Balloon, Coronary↗
PubMed1994

Intravenous Fluosol in the treatment of acute myocardial infarction. Results of the Thrombolysis and Angioplasty in Myocardial Infarction 9 Trial. TAMI 9 Research Group.

BACKGROUND: This study was performed to determine the safety and potential efficacy of an intravenous perfluorochemical emulsion (Fluosol) as an adjunct reperfusion therapy aimed at preventing reperfusion injury for patients with acute myocardial infarction. METHODS AND RESULTS: Patients (430) were randomized in a prospective open-labeled study, 213 to receive Fluosol and 217 to receive no Fluosol, along with 100 mg of tissue-type plasminogen activator given over 3 hours. Major end points included global ejection fraction, regional wall motion analysis, infarct size as measured by tomographic thallium imaging, and a composite clinical outcome measure. Baseline patient and angiographic characteristics were similar in the two groups. No significant difference in global ejection fraction (52% without Fluosol, 51% with Fluosol) or regional wall motion (-2.4 SD/chord with Fluosol, -2.2 SD/chord without Fluosol) was demonstrated in patients receiving Fluosol versus those not receiving Fluosol, nor was there a significant difference in thallium infarct size. Although Fluosol-treated patients with anterior infarction had an insignificantly lower mean infarct size (18.7% of the left ventricle) compared with patients with anterior infarction not treated with Fluosol (21.2% of left ventricle), this trend was not evident in the median infarct size values (22% versus 17%), left ventricular ejection fraction values (46% without Fluosol, 47% with Fluosol), or regional wall motion (-2.5 SD/chord in both groups). Rates of death and stroke were no different in the two groups; however, patients who received Fluosol experienced less recurrent ischemia. Patients receiving intravenous Fluosol had more transient congestive heart failure and pulmonary edema, perhaps because of necessary fluid administration. There was no difference in hemorrhagic complications between the two study groups. CONCLUSIONS: When given with a thrombolytic agent, Fluosol was not associated with improvement in ventricular systolic function, reduction in thallium infarct size, or overall clinical outcome. Fluosol was, however, associated with a reduction in ischemic complications and with an increase in pulmonary edema and congestive heart failure.

Adolescent↗
PubMed1999

Association between myocardial infarction and the mast cells in the adventitia of the infarct-related coronary artery.

BACKGROUND: Histamine, a product of mast cells, is an effective vasoconstrictor of atherosclerotic coronary arteries. Because it has been suggested that coronary spasm plays a role in acute coronary syndromes such as myocardial infarction (MI), we quantified and characterized the mast cells in the adventitia of infarct-related coronary arteries. METHODS AND RESULTS: In a series of 17 autopsied MI patients, we identified the segment of the left coronary artery with ruptured plaque responsible for the infarction. More distal segments from the infarct-related coronary artery, either with nonruptured plaques or with normal intima, were also studied. Corresponding segments taken from left coronary arteries obtained from 17 patients who had died of noncardiac causes served as controls. Adventitial mast cells in the infarct-related and the control coronary arteries were identified immunohistochemically by staining for tryptase. In the infarct-related coronary arteries, we also stained for chymase and histamine. Moreover, T lymphocytes and macrophages were identified immunohistochemically and counted. In the infarct-related coronary arteries, significantly larger numbers of mast cells were present in the adventitia backing ruptured plaques (98+/-40 mast cells/mm2, mean+/-SD) than in the adventitia backing nonruptured plaques (41+/-12 mast cells/mm2; P<0.001) or backing normal intima (19+/-8 mast cells/mm2; P<0.001). No such difference was found among the 3 different segments in the control coronary arteries. The majority of mast cells contained not only tryptase but also chymase. Mast cells were the only cells in the coronary adventitia that contained histamine. The proportion of adventitial mast cells that were degranulated was highest in the segments with ruptured plaques. The numbers of adventitial macrophages and T lymphocytes were also increased in the segments with plaque rupture. CONCLUSIONS: In infarct-related coronary arteries, the number of degranulated mast cells in the adventitia backing ruptured plaques is increased. Histamine released from the degranulated mast cells may reach the media, where it may locally provoke coronary spasm and thus contribute to the onset of MI.

Aged↗
PubMed2005

Shape and volume of lacunar infarcts: a 3D MRI study in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy.

BACKGROUND AND PURPOSE: The shape and exact size of lacunar infarcts have been investigated only postmortem. Recent imaging techniques based on triangulation and connectivity can now be used for 3D segmentation of cerebral lesions. The shape and size of lacunar infarcts was investigated using these techniques in 10 cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) patients. METHODS: We segmented 102 lacunar infarcts on T1-weighted images. The surface of the corresponding set of voxels was computed as a mesh of triangles. Thereafter, the shape of each lesion in 3D was visually analyzed by 2 investigators. RESULTS: The volume of lesions ranged from 10.5 to 1146 mm, with 93% of them having a volume <500 mm; 83% lacunar infarcts had a spheroid or ovoid shape, but 17% presented as sticks, slabs, or with a complex shape. Lesions with multiple components appeared larger than the others, and a tail extension was noticed in 13 of 102 lesions. CONCLUSIONS: These results suggest the following: (1) most lacunar infarcts in CADASIL have a volume far below one third of that of a sphere of 15 mm in diameter, the upper limit currently used for their identification on 2D imaging; (2) a significant proportion of lacunar infarcts have a shape distinct from the spheroid-ovoid morphology; and (3) lesions with a complex shape may result from the involvement of the largest small arteries, confluence of ischemic lesions, or secondary tissue degeneration. The segmentation of lacunar infarcts appears promising to better understand the pathophysiology of tissue lesions secondary to small vessel diseases.

Aged↗
PubMed1993

Clinical and angiographic features of patients with an occluded versus a patent infarct vessel after intravenous streptokinase for acute myocardial infarction.

Despite early treatment with thrombolytic agents for acute myocardial infarction, a significant portion of patients fail to achieve a patent infarct artery. To study the various factors related to achieving patency in the infarct vessel, 201 patients who received streptokinase within six hours of symptoms were studied. All patients underwent cardiac catheterization during the same hospitalization at 5.40 +/- 3.26 days after admission. Forty-five (22.4%) patients were found to have an occluded infarct artery (group 1) and 156 (77.6%) had a patent infarct vessel (group 2). There was no difference in the time from onset of symptoms to receiving streptokinase between the two groups. The two groups were similar to each other with regard to age, gender, history of myocardial infarction or angina, and major risk factors for coronary disease. Coagulation parameters before and after streptokinase therapy, reflecting the lytic state, were similar in both groups. The left ventricular end diastolic pressure was significantly higher and the left ventricular ejection fraction was significantly lower in group 1 than in group 2. These observations suggest that despite early initiation of thrombolytic therapy in patients with acute myocardial infarction, a significant portion of patients fail to achieve a patent infarct artery. This failure cannot be explained by the observed clinical parameters or the lytic state after streptokinase.

Adult↗
PubMed1999

Basic fibroblast growth factor increases regional myocardial blood flow and salvages myocardium in the infarct border zone in a rabbit model of acute myocardial infarction.

Basic fibroblast growth factor (bFGF) has been shown by some to promote angiogenesis and myocardial salvage in experimentally induced acute myocardial infarction. Although these findings have spurred much clinical interest, they are not universally observed, and the true efficacy of bFGF remains unclear. The authors used a rabbit model of acute myocardial infarction to further elucidate the effects of bFGF on acutely infarcted myocardium containing few collaterals. Myocardial infarction was evoked by ligation of the left coronary artery. Prior to ligation, either 100 microg of bFGF (bFGF group; n = 15) or physiological saline (control group; n = 22) was injected into the myocardium supplied by the ligated artery. With use of nonradioactive colored microspheres, regional blood flow (Qm) was measured before, immediately after, and 4 weeks after coronary artery ligation. Infarct and border zone sizes were measured in cross-sectional slices of the resected hearts, and the amount of viable myocardium (myocardium score) and the extent of fibrosis were histologically determined in each area. Four weeks after ligation, Qm values in the infarcted area did not significantly differ between the bFGF and control groups (0.54 +/- 0.36 vs 0.48 +/- 0.30 mL/min/g); in the border zone, Qm tended to be higher in the bFGF group (3.39 +/- 2.68 vs 1.47 +/- 0.80 mL/min/g), but the difference was not significant; finally in the noninfarcted area, Qm was significantly (p < 0.05) higher in the bFGF group (6.06 +/- 3.85 vs 2.09 +/- 0.82 mL/min/g). There was no significant difference in the amount of viable myocardium or the extent of fibrosis in the infarcted areas of the two groups. In the border zone, however, the amount of viable myocardium was significantly (p < 0.005) larger in the bFGF group (61.8 +/- 8.5% vs 35.8 +/- 20.3% of the visual field). Likewise, as graded on a scale from 0 to 5, the extent of fibrosis was significantly (p < 0.005) less in the bFGF group (2.1 +/- 0.5 vs 3.3 +/- 0.8). In conclusion, injection of bFGF into acutely infarcted myocardium increased blood flow to the noninfarcted area and salvaged the myocardium in the border zone.

Animals↗
PubMed2005

Can pulsed ultrasound increase tissue damage during ischemia? A study of the effects of ultrasound on infarcted and non-infarcted myocardium in anesthetized pigs.

BACKGROUND: The same mechanisms by which ultrasound enhances thrombolysis are described in connection with non-beneficial effects of ultrasound. The present safety study was therefore designed to explore effects of beneficial ultrasound characteristics on the infarcted and non-infarcted myocardium. METHODS: In an open chest porcine model (n = 17), myocardial infarction was induced by ligating a coronary diagonal branch. Pulsed ultrasound of frequency 1 MHz and intensity 0.1 W/cm2 (ISATA) was applied during one hour to both infarcted and non-infarcted myocardial tissue. These ultrasound characteristics are similar to those used in studies of ultrasound enhanced thrombolysis. Using blinded assessment technique, myocardial damage was rated according to histopathological criteria. RESULTS: Infarcted myocardium exhibited a significant increase in damage score compared to non-infarcted myocardium: 6.2 +/- 2.0 vs. 4.3 +/- 1.5 (mean +/- standard deviation), (p = 0.004). In the infarcted myocardium, ultrasound exposure yielded a further significant increase of damage scores: 8.1 +/- 1.7 vs. 6.2 +/- 2.0 (p = 0.027). CONCLUSION: Our results suggest an instantaneous additive effect on the ischemic damage in myocardial tissue when exposed to ultrasound of stated characteristics. The ultimate damage degree remains to be clarified.

Animals↗
PubMed1992

Centrum ovale infarcts: subcortical infarction in the superficial territory of the middle cerebral artery.

The centrum ovale, which contains the core of the hemispheric white matter, receives its blood supply from the superficial (pial) middle cerebral artery (MCA) system through perforating medullary branches (MBs), which course toward the lateral ventricles. Though vascular changes in the centrum ovale have been emphasized in dementia, stroke from acute infarction in the centrum ovale is less well documented. We studied 36 patients with infarct limited to MB territory, without involvement of the lenticulostriate territory. Ten patients had a large infarct, associated with severe disease of the ipsilateral carotid artery and with neurologic-neuropsychological impairment not different from that of large MCA infarcts. In 26 patients, the infarct was small and round or ovoid, and was associated with hypertension or diabetes and with "lacunar syndromes," usually of progressive onset. These findings show that two forms of centrum ovale infarcts can be delineated according to infarct size and shape, clinical picture, risk factors, and associated vascular disease. We propose to classify subcortical infarcts in the carotid system into four main territory groups: (1) deep perforator territory (from the MCA trunk, carotid siphon, anterior choroidal artery, anterior cerebral artery trunk, Heubner's artery, and posterior communicating artery); (2) perforating MB territory (from the superficial MCA branches); (3) junctional (territory between 1 and 2); and (4) combined territories.

Aged↗
PubMed2004

Increases in interleukin-6 and matrix metalloproteinase-9 in the infarct-related coronary artery of acute myocardial infarction.

BACKGROUND: To elucidate the involvement of inflammation in coronary artery occlusion, the regional changes in cytokines and matrix metalloproteinases (MMPs) in the infarct-related coronary artery were determined in patients with acute myocardial infarction. METHODS AND RESULTS: Cardiac catheterization was carried out within 24 h of the onset of infarction in 36 patients. Blood samples were collected from the infarct-related coronary artery, the ascending aorta and the peripheral vein. Plasma interleukin (IL)-6 concentrations were elevated in all 3 samples. Particularly, the plasma IL-6 concentrations were 14.4 pg/ml in the infarct-related coronary artery, a value significantly greater than the respective 8.0 pg/ml and 6.5 pg/ml in the ascending aorta and peripheral vein. Plasma IL-6 concentrations in the infarct-related coronary artery had positive correlation with all of the following references measured by intravascular ultrasound: external elastic membrane cross-sectional area (EEM-CSA) (r=0.47, p<0.01), lesion EEM-CSA (r=0.51, p<0.01) and plaque area (r=0.48, p<0.01). MMP-9 was increased regionally in the infarct-related coronary artery, at 11.8 ng/ml vs 8.2 ng/ml in the ascending aorta (p<0.001). CONCLUSIONS: The present findings suggest that IL-6 at least is released from the ruptured vulnerable atherosclerotic plaque and that regional activation of macrophages is involved in the occlusive process of coronary artery in acute myocardial infarction.

Adult↗
PubMed1996

Sequential changes in laminin and type IV collagen in the infarct zone--immunohistochemical study in rat myocardial infarction.

BACKGROUND: The healing process, which affects ventricular remodeling, is an important factor in the prognosis of myocardial infarction. We hypothesized that laminin and type IV collagen contribute to extracellular matrix assembly in healing after myocardial infarction. We examined sequential changes in these two components after experimental myocardial infarction in rats. MATERIALS AND METHODS: Hearts were excised from 1 day to 10 weeks after permanent left coronary ligation in rats. Immunohistochemical staining with a polyclonal antibody to laminin and type IV collagen was performed by the avidin-biotin-peroxidase method. RESULTS: Laminin: On day 3, laminin initially appeared in a wavy fashion in the granulation tissue of the infarct peripheral zone and was not restricted to the cell membrane; the staining distribution in the peripheral zone then gradually increased, reaching a maximum on days 7-11. The distribution progressed from the peripheral zone to the outer lesion of the central zone of the infarct for 1-2 days, and reached the center point after 2 weeks. The extent of the staining distribution gradually decreased after reaching this maximum, but the staining did not completely disappear. Type IV Collagen: Changes in type IV collagen were essentially the same as those in laminin. A wavy staining pattern of type IV collagen appeared in the infarct peripheral zone from day 3, reached its maximum extent on days 7-11, and decreased gradually thereafter. The distribution progressed from the peripheral zone to the outer lesion of the central zone for 1-2 days, reaching the center point after 2 weeks. CONCLUSIONS: Laminin and type IV collagen contribute to extracellular matrix formation in the infarct zone relatively early after myocardial infarction.

Animals↗
PubMed1999

Postmortem evaluation of morphologic changes in the infarcted myocardium that predict ventricular septal rupture in acute anteroseptal infarction.

Although thinning of the ventricular wall due to infarct expansion (septal aneurysm) may contribute to ventricular septal rupture (VSR), spatial factors predisposing to this mechanical complication have not been fully demonstrated. To identify the morphologic predictors of VSR, a retrospective postmortem study was performed on 17 hearts with acute anteroseptal myocardial infarction, comprising 7 with VSR and 10 without rupture. Infarct size and the extent of wall thinning were quantified. Wall thinning was defined as a decrease of less than 50% of thickness of the noninfarcted wall. The total infarct size did not differ among the groups. In the free wall (FW), the infarct was smaller in hearts with VSR than in those with a ruptured FW (p<0.05) or no rupture (p<0.01). The septal involvement was more extensive in patients with VSR than in those with FW rupture (p<0.05). Septal thinning was more extensive in hearts with VSR than in those with FW rupture (p<0.05) or non-rupture (p<0.05). A combination of a small infarct of the FW and a large septal infarct may contribute to the formation of septal aneurysm, which is believed to predispose to VSR. The presence of a small infarct of the anterior septum may be another setting for postinfarction septal rupture.

Aged↗
PubMed2003

Effect of pre-infarction angina on ventricular late potentials in patients with acute myocardial infarction and successful thrombolysis.

OBJECTIVE: Pre-infarction angina is considered as a good clinical model of ischaemic preconditioning which facilitates myocardial protection. Late potentials (LP) have prognostic significance following acute myocardial infarction (AMI). It is also well established that thrombolytic therapy reduces the incidence of LP. Our aim was to evaluate the relationship between pre-infarction angina and LP in patients receiving successful thrombolytic therapy. METHODS AND RESULTS: We prospectively studied 55 patients presenting with AMI (<6 hours). All patients received thrombolytic therapy and were evaluated with coronary angiography at predischarge. Signal-averaged recordings (SAECG) were obtained serially prior to thrombolysis, 48 hours after and 10 days later. Pre-infarction angina was present in 14 (25%) patients. There were no significant differences between the clinical characteristics and angiographic findings of the groups. Baseline SAECG parameters of the groups were also similar. After thrombolysis, the 48th hour values of LAS (the duration of the terminal low amplitude signals), and both the 10th day values of LAS and RMS (root mean square voltage of the last 40 ms of the QRS) were significantly better in the pre-infarction angina group. The mean filtered QRS duration and RMS 40 values changed significantly at the 10th day recordings of patients with pre-infarction angina [QRS duration, 110+/-34 ms before to 91+/-11 ms after (p = 0.039); RMS 40, 40+/-17 microV before to 50+/-14 microV after (p = 0.02)]. The incidence of LP significantly decreased after thrombolytic therapy in the pre-infarction angina group, however, this change was not observed in patients without angina. CONCLUSION: Presence of pre-infarction angina reduces the incidence of LP following thrombolysis in AMI. This might be explained by the possible beneficial effect of ischaemic preconditioning on the arrhythmogenic substrate.

Action Potentials↗
PubMed1991

Acute phase reaction, infarct size and in-hospital morbidity in myocardial infarction patients treated with streptokinase or recombinant tissue type plasminogen activator.

We examined the acute phase reaction in myocardial infarction after thrombolytic treatment by streptokinase or tissue plasminogen activator. The magnitude of the acute phase reaction as determined by measurements of serum C-reactive protein and amyloid-A protein did not correlate with infarct size (determined by serial measurements of creatine kinase-MB) in this patient population. On the other hand, the development of acute cardiac failure was more closely associated with the magnitude of the acute phase reaction than with infarct size. The peak serum values of C-reactive protein in patients with and without acute cardiac failure were 128 mg/l (95% confidence intervals 85-170) and 60 mg/l (30-89); P less than 0.01 and concentration time integrals 578 mg/l x days (368-787) and 205 mg/l x days (62-350); P less than 0.01. The corresponding creatine kinase-MB values were 310 U/l (191-429) and 207 U/l (125-289) not significant; and 319 U/l x days (201-437) and 204 U/l x days (124-286) not significant; respectively. Patients requiring medication for cardiac failure on discharge from hospital had higher C-reactive protein and serum amyloid A protein values than those who did not, although the difference did not quite reach statistical significance. The infarct sizes were similar whether the patients needed medication for cardiac failure at discharge or not. Subjectively felt morbidity due to myocardial infarction was linearly associated with serum C-reactive protein peak values (P less than 0.05) and concentration time integrals (P less than 0.05), but not with infarct size. We conclude that thrombolytic treatment of myocardial infarction may reduce hospital inpatient morbidity independently of the limitation of infarct size. This diminished morbidity seems to be associated with modest or low acute phase reaction.

Acute-Phase Reaction↗
PubMed1990

Effect of intravenous streptokinase on early mortality in patients with suspected acute myocardial infarction. A meta-analysis by anatomic location of infarction .

PURPOSE: To determine the effect of intravenous streptokinase on early mortality in patients with suspected acute anterior and acute inferior myocardial infarctions. DATA IDENTIFICATION: A literature search of English-language studies on the use of intravenous streptokinase in the treatment of suspected acute myocardial infarction for the period 1966 to 1989 using Medlars II and the bibliographies of relevant articles. In a number of instances, additional details on early mortality by location of myocardial infarction were provided by the authors. STUDY SELECTION: Of 140 originally identified articles, 6 that specifically met our inclusion criteria were selected: randomized trials that used intravenous streptokinase in a dose of 1.5 million units, with or without additional agents, compared with a group that differed only by the absence of streptokinase. Trials were selected by review of the methods section without regard for the results. DATA EXTRACTION: Data were extracted independently by two observers using specific methodologic criteria for infarct location and early mortality. After they conferred, the observers agreed completely on the data. RESULTS OF DATA SYNTHESIS: Among the 9155 patients with suspected acute anterior myocardial infarction, the mortality rate in the control group was 17.4%. In contrast, patients treated with streptokinase had a 12.5% mortality. The mean risk difference was -4.8% (95% CI, -7.5% to -2.1%) and the summary risk ratio was 0.72 (CI, 0.65 to 0.79). A total of 9650 patients with suspected inferior infarction had a mortality rate in the control group of 7.6% [corrected]. The mortality for streptokinase-treated patients was 6.6%. The mean risk difference was -0.8% (CI, -1.8% to 0.2%) and the summary risk ratio was 0.87 (CI, 0.76 to 1.01). CONCLUSIONS: Intravenous streptokinase clearly confers a protective effect against early mortality in patients with suspected acute anterior myocardial infarction. The magnitude of this effect is on the order of a 5% absolute reduction in risk of death by 21 to 35 days. For these patients, 21 need to be treated to save 1 additional life. For patients with suspected acute inferior infarction, the benefit of treatment on reducing early mortality is of smaller magnitude and less certain. These patients have an estimated absolute reduction of early mortality of approximately 1%, which would require treating 125 patients to save 1 additional life.

Humans↗