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PubMed1994

Sex differences in the management and long-term outcome of acute myocardial infarction. A statewide study. MIDAS Study Group. Myocardial Infarction Data Acquisition System.

BACKGROUND: We wished to evaluate whether differences in the rate of invasive cardiac procedures between men and women with acute myocardial infarction are associated with different short- and long-term mortality. METHODS AND RESULTS: The database (Myocardial Infarction Data Acquisition System, MIDAS) included all discharges for the years 1986 and 1987 with the diagnosis of acute myocardial infarction in New Jersey, based on the New Jersey hospital discharge data system (MIDS/UB-82). Accuracy of the data was evaluated by auditing 726 randomly selected charts. The variables examined included age, sex, race, comorbidity (anemia, chronic liver disease, cancer, chronic obstructive pulmonary disease, diabetes, hypertension, prior myocardial infarction), complications (left ventricular dysfunction, arrhythmias, conduction defects), insurance status, performance of cardiac catheterization, percutaneous transluminal coronary angioplasty, or coronary artery bypass graft surgery, and survival up to 3 years. Women were older, had longer hospital stay, and were more likely than men to have anemia, diabetes, hypertension, left ventricular dysfunction, and Medicare or Medicaid insurance coverage. They were less likely than men to be admitted to a hospital equipped to perform invasive procedures or to have chronic obstructive pulmonary disease, chronic liver disease, prior myocardial infarction, or arrhythmias. After adjustment for these differences, women were less likely than men to have cardiac catheterization. Cardiac catheterization was associated with lower mortality. Women up to age 70 had higher 3-year death rates than men after adjustment for age, race, comorbidity, complications, and insurance type. This difference between men and women was somewhat diminished after the performance of cardiac catheterization and revascularization was taken into account. Unadjusted mortality was high in this study group. CONCLUSIONS: Women with acute myocardial infarction are less likely to have invasive cardiac procedures and have higher 3-year adjusted death rate up to age 70 than men.

Aged↗

PubMed1997

Collagen scar formation after acute myocardial infarction: relationships to infarct size, left ventricular function, and coronary artery patency.

BACKGROUND: Left ventricular function after acute myocardial infarction (AMI) is determined by the expansion of the infarct zone and remodeling of the noninfarcted myocardium. An occluded infarct-related artery (IRA) is an independent risk factor for remodeling. METHODS AND RESULTS: Changes in myocardial collagen metabolism were evaluated in 36 patients with suspected AMI. The plasma creatine kinase MB fraction and myoglobin release curves were analyzed for assessment of early reperfusion and infarct size. Collagen scar formation was evaluated by measurement of serum concentrations of the aminoterminal propeptide of type III procollagen (PIIINP), the aminoterminal propeptide of type I procollagen (intact PINP), and the carboxyterminal propeptide of type I procollagen (PICP). Plasma renin activity and urine excretion of cortisol and aldosterone were also measured. Coronary angiography and left ventricular cineangiography were performed during early hospitalization. The serum concentration of PIIINP increased from 3.50+/-0.20 to a maximum of 5.08+/-0.36 microg/L (n=32) in the patients with AMI, whereas the concentrations of intact PINP and PICP tended to decrease. The area under the curve (AUC) of PIIINP during the first 10 postinfarction days was larger in patients with severe heart failure or ejection fractions < or = 40% than in those with no heart failure or with an ejection fraction > 40% (P<.05 and P<.01, respectively), and it was also larger in the patients with TIMI grade 0 to 2 flows than in those with TIMI 3 flows (P<.05), despite similar enzymatically determined infarct sizes. No significant correlations between PIIINP and neurohumoral parameters were observed. The AUC of PIIINP and the change in PIIINP during the first 4 days were significantly correlated with indices of cardiac function. CONCLUSIONS: Collagen scar formation after AMI can be quantified by measurement of serum PIIINP concentrations. Scar formation is more prominent in large infarctions causing left ventricular dysfunction and in patients with occluded IRAs.

Adult↗

PubMed1990

Evidence against the "early protection-delayed death" hypothesis of superoxide dismutase therapy in experimental myocardial infarction. Polyethylene glycol-superoxide dismutase plus catalase does not limit myocardial infarct size in dogs.

We previously found that superoxide dismutase (SOD) did not limit myocardial infarct size after 40 or 90 minutes of ischemia and 4 days of reperfusion in dogs. Because some other studies have shown limitation of infarct size after shorter periods of reperfusion, we postulated that our negative results might be due to late reperfusion injury mediated by superoxide anions produced after excretion of SOD. To test this "early protection-delayed death" hypothesis, we have examined whether SOD, conjugated to polyethylene glycol (PEG-SOD) to prolong its circulating half-life, limited myocardial infarct size. The circumflex artery was occluded for 90 minutes followed by 4 days of reperfusion. PEG-SOD (total dose, 10,000 units/kg) and catalase (55,000 units/kg) were given during the 30 minutes before reperfusion. Plasma SOD levels in the treated group were 330 +/- 20 units/ml at the onset of reperfusion and 140 +/- 10 units/ml on day 4 (circulating half-life, 75 +/- 5 hours) versus 5 +/- 1 units/ml in controls. Histological infarct size was 37.1 +/- 4.2% of the area at risk in the treated group (n = 11) versus 44.5 +/- 6.2% in controls (n = 10) (p = NS). Infarct size and collateral blood flow were inversely related in controls; PEG-SOD and catalase did not shift this regression (p = NS by analysis of covariance). Thus, infarct size was not limited when measured after 4 days of reperfusion, even though plasma SOD exceeded 100 units/ml throughout this reperfusion period.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2005

Prevention of left ventricular remodeling with granulocyte colony-stimulating factor after acute myocardial infarction: final 1-year results of the Front-Integrated Revascularization and Stem Cell Liberation in Evolving Acute Myocardial Infarction by Granulocyte Colony-Stimulating Factor (FIRSTLINE-AMI) Trial.

BACKGROUND: Experimental and clinical evidence has recently shown that pluripotent stem cells can be mobilized by granulocyte colony-stimulating factor (G-CSF) and may enhance myocardial regeneration early after primary percutaneous coronary intervention (PCI) management of acute myocardial infarction. Sustained or long-term effects of mobilized CD34-positive mononuclear stem cells, however, are unknown. METHODS AND RESULTS: Thirty consecutive patients with ST-elevation myocardial infarction undergoing primary PCI with stenting and abciximab were selected for the study 85+/-30 minutes after PCI; 15 patients were randomly assigned to receive subcutaneous G-CSF at 10 microg/kg body weight for 6 days in addition to standard care including aspirin, clopidogrel, an angiotensin-converting enzyme inhibitor, beta-blocking agents, and statins. In patients with comparable demographics and clinical and infarct-related characteristics, G-CSF stimulation led to sustained mobilization of CD34 positive mononuclear cells (MNC(CD34+)), with a 20-fold increase (from 3+/-2 at baseline to 66+/-54 MNC(CD34+)/microL on day 6; P<0.001); there was no evidence of leukocytoclastic effects, accelerated restenosis rate, or any late adverse events. Within 4 months, G-CSF-induced MNC(CD34+) mobilization led to enhanced resting wall thickening in the infarct zone of 1.16+/-0.29 mm (P<0.05 versus control), which was sustained at 1.20+/-0.28 after 12 months (P<0.001 versus control). Similarly, left ventricular ejection fraction improved from 48+/-4% at baseline to 54+/-8% at 4 months (P<0.005 versus control) and 56+/-9% at 12 months (P<0.003 versus control and paralleled by sustained improvement of wall-motion score index from 1.70+/-0.22 to 1.42+/-0.26 and 1.33+/-0.21 at 4 and 12 months, respectively), after G-CSF (P<0.05 versus baseline and P<0.03 versus controls). Accordingly, left ventricular end-diastolic diameter showed no remodeling and stable left ventricular dimensions after G-CSF stimulation, whereas left ventricular end-diastolic diameter in controls revealed enlargement from 55+/-4 mm at baseline to 58+/-4 mm (P<0.05 versus baseline) at 12 months after infarction and no improvement in diastolic function. CONCLUSIONS: Mobilization of MNC(CD34+) by G-CSF after primary PCI may offer a pragmatic strategy for improvement in ventricular function and prevention of left ventricular remodeling 1 year after acute myocardial infarction.

Abciximab↗

PubMed2006

Stem cell mobilization induced by subcutaneous granulocyte-colony stimulating factor to improve cardiac regeneration after acute ST-elevation myocardial infarction: result of the double-blind, randomized, placebo-controlled stem cells in myocardial infarction (STEMMI) trial.

BACKGROUND: Phase 1 clinical trials of granulocyte-colony stimulating factor (G-CSF) treatment after myocardial infarction have indicated that G-CSF treatment is safe and may improve left ventricular function. This randomized, double-blind, placebo-controlled trial aimed to assess the efficacy of subcutaneous G-CSF injections on left ventricular function in patients with ST-elevation myocardial infarction. METHODS AND RESULTS: Seventy-eight patients (62 men; average age, 56 years) with ST-elevation myocardial infarction were included after successful primary percutaneous coronary stent intervention <12 hours after symptom onset. Patients were randomized to double-blind treatment with G-CSF (10 microg/kg of body weight) or placebo for 6 days. The primary end point was change in systolic wall thickening from baseline to 6 months determined by cardiac magnetic resonance imaging (MRI). An independent core laboratory analyzed all MRI examinations. Systolic wall thickening improved 17% in the infarct area in the G-CSF group and 17% in the placebo group (P=1.0). Comparable results were found in infarct border and noninfarcted myocardium. Left ventricular ejection fraction improved similarly in the 2 groups measured by both MRI (8.5 versus 8.0; P=0.9) and echocardiography (5.7 versus 3.7; P=0.7). The risk of severe clinical adverse events was not increased by G-CSF. In addition, in-stent late lumen loss and target vessel revascularization rate in the follow-up period were similar in the 2 groups. CONCLUSIONS: Bone marrow stem cell mobilization with subcutaneous G-CSF is safe but did not lead to further improvement in ventricular function after acute myocardial infarction compared with the recovery observed in the placebo group.

Adult↗

PubMedDate not supplied

Association between depressive episode before first myocardial infarction and worse cardiac failure following infarction.

Depression following myocardial infarction is associated with a higher mortality rate. The authors studied 314 patients admitted to the hospital with a first myocardial infarction to assess whether cardiac failure after the infarction, which is also linked to a higher mortality rate, was predicted by psychosocial characteristics present before the myocardial infarction. One-fifth (20.7%) of the subjects met the ICD-10 criteria for depressive episode in the 1 month before the attack. Variables independently associated with worse cardiac failure after the myocardial infarction were greater age, a history of angina preceding the infarction, and a previous depressive episode. The impact of depression on postinfarction outcome may result from the influence of preinfarction depression on the degree of cardiac failure.

Depression↗

PubMed2002

Lymph node infarction associated with infectious mononucleosis: report of a case resembling lymph node infarction associated with malignant lymphoma.

A completely infarcted lymph node should alert the pathologist to the high possibility of malignant lymphoma. The lymph node lesion of infectious mononucleosis (IM) shows marked histologic diversity and occasionally may be confused with malignant lymphoma. We report a rare case of IM showing extensive lymph node infarction whose lymph node lesion was similar to lymph node infarction associated with malignant lymphoma. This case describes a 32-year-old Japanese man who had signs and symptoms consistent with IM, which he was later proven serologically to have, but whose cervical lymph node showed extensive lymph node infarction with a thin area of granulation tissue beneath the capsule. The infarcted tissue contained numerous eosinophilic ghosts of large lymphoid cells. The thin granulation tissue was composed of numerous small lymphocytes, plasma cells, and histiocytes, in addition to large lymphoid cells including immunoblasts and granulocytes. CD20, CD3, and CD45RO immunostains revealed the mixed B- and T-cell nature of the ghosts of large lymphoid cells in the infarcted tissue as well as viable large cells in the granulation tissue. The patient was free from disease after 50 months' follow-up.

Adult↗

PubMed1985

Effects of propranolol on infarct size and the impaired hemodynamics in experimental myocardial infarcted dogs.

We studied the effects of propranolol on infarct size and hemodynamic impairment induced by 24 h-coronary ligation. The myocardial infarction produced by the left circumflex coronary artery ligation was more consistent than that induced by the left anterior descending coronary artery ligation, suggesting that the former is a more appropriate experimental model for pharmacological evaluations. Oral treatment with propranolol, 3-30 mg/kg, reduced infarct size and reduced the elevated left ventricular end-diastolic pressure, which was shown to be most closely related with infarct size, in dogs with circumflex coronary artery ligation extending over 24 h. In conclusion, our results indicate that propranolol protects against the enlargement of infarct size and improves the impaired hemodynamics observed in myocardial infarcted dogs with occlusions extending over 24 h, as well as in dogs with less than 24 h-occlusions reported by numerous investigators.

Administration, Oral↗

PubMed2004

Rationale and design of a large-scale trial using nicorandil as an adjunct to percutaneous coronary intervention for ST-segment elevation acute myocardial infarction: Japan-Working groups of acute myocardial infarction for the reduction of Necrotic Damage by a K-ATP channel opener (J-WIND-KATP).

BACKGROUND: The benefits of percutaneous coronary intervention (PCI) in acute myocardial infarction (AMI) are limited by reperfusion injury. In animal models, nicorandil, a hybrid of an ATP-sensitive K(+) (KATP) channel opener and nitrates, reduces infarct size, so the Japan-Working groups of acute myocardial Infarction for the reduction of Necrotic Damage by a K-ATP channel opener (J-WIND-KATP) designed a prospective, randomized, multicenter study to evaluate whether nicorandil reduces myocardial infarct size and improves regional wall motion when used as an adjunctive therapy for AMI. METHODS AND RESULTS: Twenty-six hospitals in Japan are participating in the J-WIND-KATP study. Patients with AMI who are candidates for PCI are randomly allocated to receive either intravenous nicorandil or placebo. The primary end-points are (1) estimated infarct size and (2) left ventricular function. Single nucleotide polymorphisms (SNPs) that may be associated with the function of KATP-channel and the susceptibility of AMI to the drug will be examined. Furthermore, a data mining method will be used to design the optimal combined therapy for post-myocardial infarction (MI) patients. CONCLUSIONS: It is intended that J-WIND-KATP will provide important data on the effects of nicorandil as an adjunct to PCI for AMI and that the SNPs information that will open the field of tailor-made therapy. The optimal therapeutic drug combination will also be determined for post-MI patients.

Adult↗

PubMed2004

Multi-detector computed tomography for imaging of subendocardial infarction: prediction of wall motion recovery after reperfused anterior myocardial infarction.

BACKGROUND: After reperfusion therapy for acute myocardial infarction (AMI), evaluation of transmural myocardial microcirculation can indicate prognosis. The aim of the present study was to determine whether the evaluation of transmural myocardial microcirculation by newly developed 4-slice computed tomography (CT) can estimate the recovery of left ventricular function. METHODS AND RESULTS: Seventeen consecutive patients who had anterior AMI with a total occlusion in the proximal left anterior descending artery (LAD) and who had undergone successful balloon reperfusion therapy within 24 h of the onset of AMI were examined. Four-slice CT was performed 10-14 days after AMI onset. The median of the epicardial perfusion ratio (infarcted anterior epicardial CT number/intact lateral epicardial CT number ratio = 92%) was used to categorize the cases into 2 groups: the transmural infarction group (n=8) and the subendocardial infarction group (n=9). Although no significant difference was observed between myocardial enhancement by CT in the acute phase and anterior wall motion or ejection fraction in the acute phase, the transmural infarction group showed poor recovery of anterior wall motion at 6 months after AMI onset, whereas the subendocardial infarction group exhibited good recovery of regional and global left ventricular function. CONCLUSIONS: Transmural myocardial microcirculation imaged by 4-slice CT can predict wall motion recovery after AMI.

Angioplasty, Balloon↗

PubMed1981

The reappraisal fo ST segment elevation as an index of infarct size in patients with acute anterior myocardial infarction.

The clinical meaning or precordial ST segment mapping for assessment of infarct size was studied in 12 patients with acute anterior myocardial infarction. sigma ST39 (the sum of ST segment elevations in 39 precordial leads), sigma STV1--6 (the sum of ST segment elevations in the standard chest leads) and STMAX (the maximum of ST segment elevation in 39 precordial leads) were obtained serially after the onset from precordial electrocardiographic mapping records. The infarct size and the time (Tf) when the evolution of myocardial infarction finished were calculated by the total creatine phosphokinase released (sigma CPK) and serial changes in CPK releasing rate, respectively. sigma STV1--6 at Tf, as closely as sigma ST39 (r = 0.82, p less than 0.01), correlated with sigma CPK (r = 0.79, p less than 0.01). Even STMAX at the time of Tf significantly correlated with sigma CPK (r = 0.60, p less than 0.05), although the correlation coefficient was not so well as the former two. These results showed that sigma STV1--6 reflected infarct size as satisfactorily as sigma ST39 and could be useful for measuring infarct size.

Creatine Kinase↗

PubMed1985

Effects of intracoronary thrombolysis on infarct size and left ventricular function in patients with anterior myocardial infarction--enzymatic, electrocardiographic, radionuclide and hemodynamic evaluations.

The influence of the duration of ischemia on infarct size and left ventricular function (LV) was assessed in 30 patients with a first anterior myocardial infarction (MI) and intracoronary thrombolysis (ICTL) on admission. The occlusion time of the left anterior descending coronary artery (LAD) was 4 hours or less in 11 patients (group I), 4-10 hours in 11 (group II) and 10 hours or more in eight (group III). Serial measurements of serum creatine kinase-MB were carried out during the acute phase. Four weeks after the procedure, electrocardiographic pathological Q waves on 34-lead precordial mapping were scored, viable left ventricular myocardial volume and the ratio of infarcted to total left ventricular myocardial volume was estimated by myocardial emission computed tomography (ECT) with thallium-201. In the acute phase enzymatic estimation of infarct size showed a significant difference between group I and the other two groups but not between groups II and III; there were no significant differences in the degree of left ventricular asynergy among the three groups. In the chronic phase infarct sizes evaluated by both Q wave mapping and ECT were smaller in group I than those in group II, which were smaller than those in group III; there were significant differences in the degree of LV asynergy among the three groups (group I less than II less than III). LV function was nearly normal in group I, moderately impaired in group II, but severely depressed in group III 4 weeks later. The present study indicates that infarct size extends and LV function deteriorates with the duration of occlusion of the LAD and that not only early (less than or equal to 4 hours) but also later (4-10 hours) reperfusion is beneficial to prevent the extension of MI and deterioration of LV function in patients with anterior MI.

Adult↗

PubMed1989

Infarct sizing after reperfusion by two-dimensional echocardiography and serum cardiac myosin light chain II in conscious dogs: dissociation between early left ventricular wall motion and ultimate infarct size.

The time course of recovery of left ventricular wall motion after coronary reperfusion and how that relates to anatomical infarct size, wall motion abnormality, and the amount of cardiac myosin light chain II release were evaluated in conscious dogs. One week after the implantation of hydraulic occluders on the left circumflex arteries, myocardial infarction was induced. Coronary reperfusion was performed 3 h after the occlusion in 9 dogs (R) and occlusion was sustained in 9 dogs (C). All dogs underwent serial 2-dimensional echocardiograms and determination of serum cardiac myosin light chain II. The infarct size was identified at 14 days. Systolic wall thickening at the center of the ischemic area (SWT) at 3 h was -7.7 +/- 2.8% (C), -9.9 +/- 3.0% (R). Systolic thinning was observed even at 14 days in C. Significant recovery of contraction was observed in R, but the improvement continued for as long as 2 days. SWT at 14 days was -1.5 +/- 2.8% (C) and 7.0 +/- 4.6% (R) (p less than 0.05). All of SWT or the extent of systolic thinning (EST) 3-hour and 14-day were correlated well with infarct size in C. In group R, 14-day SWT and 14-day EST correlated with infarct size but 3-hour SWT and 3-hour EST did not. Total release of serum cardiac myosin light chain II levels correlated well with infarct size (r = 0.88), 14-day SWT (r = -0.90) and 14-day EST (r = 0.89) in all dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Factors governing re-infarction in patients with myocardial infarction in Japan.

The subjects consisted of 2,733 patients with acute myocardial infarction (AMI) who were admitted to our 11 institutions between 1983 and 1988, examined by coronary arteriography, and discharged alive. The patients were followed for an average of 2.9 years after discharge. During the follow-up period, re-infarction occurred in 172 patients (6.3%). The factors associated with re-infarction were total cholesterol of more than 250 mg/dl, HDL-cholesterol of less than 35 mg/dl and diabetes mellitus. The rate of re-infarction was also high in patients who had had a previous infarction before admission, angina pectoris before or after the onset of AMI or multiple-vessel disease. In contrast, intracoronary thrombolysis reduced the rate of re-infarction.

Angina Pectoris↗

PubMed2001

Diagnosis of acute myocardial infarction in angiographically documented occluded infarct vessel : limitations of ST-segment elevation in standard and extended ECG leads.

STUDY OBJECTIVES: The majority of thrombolysis studies require defined ST-segment elevations as an inclusion criterion for the diagnosis of acute myocardial infarction (AMI). However, depending on the occluded infarct vessel and the criteria applied, the ECG diagnosis of AMI can be difficult to establish. Accordingly, this study was performed to evaluate the sensitivity of ST-segment elevation of standard and extended ECG leads in a cohort of patients with angiographically confirmed diagnosis of AMI. PATIENTS AND METHODS: In 418 patients (mean +/- SD age, 60 +/- 13 years) with AMI (pain onset, 4.8 +/- 3.0 h), coronary angiography with percutaneous transluminal coronary angioplasty/stenting of the culprit lesion was performed. The diagnosis of AMI was confirmed by emergency coronary angiography and laboratory analyses. ST-segment elevation (in two contiguous leads) of 1 mm in standard lead I through aVF and ST-segment elevations of 2 mm (or 1 mm, corresponding values presented in parentheses) in V(1) through V(6) were considered significant. In a subset of 102 AMI patients, additional right precordial leads V(3)R through V(6)R for evaluation of right ventricular infarction and additional chest leads V(7) through V(9) for evaluation of posterior infarction were recorded. ST-segment elevations of 1 mm in the right precordial leads and 1 mm or 0.5 mm in the posterior leads were considered significant. RESULTS: Standard leads I through V(6) showed ST-segment elevation in 85% (96%) of patients with left anterior descending artery occlusion, in 46% (61%) of patients with left circumflex coronary artery (CX) occlusion, and in 85% (90%) of patients with right coronary artery occlusion. On consideration of additional ECG tracings in the subgroup of 102 patients (V(3)R through V(6)R and V(7) through V(9)), the respective numbers increased by 2 to 8% depending on different criteria for ST-segment elevation; in patients with CX occlusion, the increase amounted to 6 to 14%. There was a trend toward an extended infarct size (maximum creatine kinase [CK] values) with concomitant ST-segment elevation in additional ECG leads as assessed by maximum CK levels. CONCLUSIONS: The sensitivity of the ECG diagnosis of AMI is only marginally increased by extended precordial chest leads. There is a trend toward an extended infarct size in those patients with concomitant ST-segment elevation in additional ECG leads.

Angioplasty, Balloon, Coronary↗

PubMed1985

Indirect measurement of infarct size. Correlative variability of enzyme, radionuclear angiographic, and body-surface-map variables in 34 patients during the acute phase of first myocardial infarction.

To gain a correlative perspective of indirect indications of the size of a myocardial infarct, we measured several body-surface electrocardiographic variables and several enzyme and radionuclear angiographic indicators of an infarct's size in 34 patients during the acute phase of first infarction. We found that bivariate correlations ranged widely, from an r value of 0.05 to an r value of 0.92, but were significantly (p less than 0.001) higher when variables from the same technique were correlated (mean r, 0.60 +/- 0.27), as opposed to correlations of variables from different techniques (mean r, 0.27 +/- 0.18). Trivariate comparisons among techniques produced significantly (p less than 0.001) higher r values, but the highest, an r value of 0.76 (total wall motion abnormality score; peak lactic dehydrogenase level; ST-segment integral maximum), indicated that even in this best case, only about 60 percent of the variation of one variable was dependent on or due to the two other variables. These data demonstrate that multiple indirect quantitative indicators of myocardial injury can vary widely in their correlations within the same population of infarcts, and much remains unknown in their relationships during the acute phase. Caution should be exercised, therefore, in their clinical application to predict an infarct's size in individual patients with acute myocardial infarction.

Adult↗

PubMed2006

Repair of post-infarct ventricular septal rupture with an infarct-exclusion technique: early results.

BACKGROUND: Ventricular septal rupture is a rare but life-threatening complication of acute myocardial infarction. The mortality rate with medical treatment is more than 90%, whereas the mortality rate after surgical repair varies between 19% and 60% in different studies. This study reviews our experience based on early closure of the septal rupture with an infarct-exclusion technique. METHODS: Eighteen consecutive patients who underwent post-infarct ventricular septal rupture operation between June 1, 2000, and November 1, 2005, were included in the study. There were 12 male and 6 female patients. Mean age was 65.72 +/- 5.21 years. All patients had echocardiography and coronary angiography before the operation. Rupture was closed with an infarct-exclusion technique in all patients. Preoperative, operative, and postoperative information were collected from patient cohorts. RESULTS: The median time from myocardial infarction to diagnosis of the ventricular septal rupture was 4.22 +/- 1.61 days. Fourteen of the patients had intra-aortic balloon pump support, and 5 had mechanic ventilator support preoperatively. Surgical repair was done 1 to 4 days after the diagnosis. Ten anterior and 8 posterior ventricular septal ruptures were found. Additional coronary artery bypass surgery was performed with a median of 1.27 +/- 0.8 grafts in 15 (83.3%) patients. The mean postoperative mechanic ventilator support time was 34.13 +/- 45.11 hours. Overall 30-day mortality was 16.7% with 3 patients. The mean intensive care unit stay was 3.3 +/- 1.6 days. Postoperative transthoracic echocardiography showed minimal residual shunts in 4 patients. CONCLUSION: Patch closure of the ventricular septal rupture with an infarct-exclusion technique provided acceptable results. Concomitant coronary artery bypass grafting might be beneficial to control additional risk of an associated coronary artery lesion. Prompt diagnosis followed by early surgical intervention is essential for patients with ventricular septal rupture.

Aged↗

PubMed1982

Quantitative assessment of infarct size in isoproterenol-infarcted rats.

The authors performed a number of experiments aiming at quantifying the infarct size in Sprague-Dawley male rats. The experimental model employed was isoproterenol (ISP) induced, infarctlike myocardial lesions. In quantifying the extent of the infarct area they compared the cross reliability of enzymatic and histological methods. ISP was administered in two subcutaneous injections (50 mg/100 Gm body weight) at a 24 hour interval. At the peak of the necrotic process (48 hrs after the first injection), the heart was subjected to enzymatic or histological studies. Thus, a group of infarcted animals (n = 25) and their controls (n = 15) underwent the assessment of creatine kinase (CK) content in the homogenate of the myocardium. Another group of animals (n = 15) was used for histological observations, including measurement of infarct size by planimetry from histological sections. A good relationship was observed between the percentage of necrotic tissue calculated on the basis of CK values (69.11 +/- 2.39%) and the infarction area assessed by planimetry (72.37 +/- 2.69%) (mean +/- standard error of the mean [SEM]). Thus, the present study confirms that ISP-induced myocardial lesions are a simple and reliable model for experimental infarct. Moreover, the assessment of the CK content in the heart is correlated with histological studies by planimetry, and is suggested as a direct enzymatic method to quantify the extent of myocardial necrosis.

Animals↗