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PubMed1990

Clinicopathological study of myocardial infarction with normal or nearly normal extracardiac coronary arteries. Quantitative analysis of contraction band necrosis, coagulation necrosis, hemorrhage, and infarct size.

In order to clarify the pathogenesis of acute myocardial infarction (MI) in hearts with normal coronary arteries, infarct size, and the extent of contraction band necrosis (CBN), coagulation necrosis, and hemorrhage were quantitatively examined using an image analyzer in 5 autopsy cases of MI with normal or nearly normal extracardiac coronary arteries. One patient died 40 h after acute MI. A second patient with acute MI due to severe spasm of segment 6, confirmed by cineangiography, died three days later. The third patient had already suffered a subarachnoid hemorrhage, and died 10 h after the onset of acute MI. The fourth patient had aortic stenosis and regurgitation. She developed acute MI due to total occlusion of segment 6, confirmed by cineangiography 4 h after the onset, and died 61 days later. Autopsy revealed old anteroseptal MI with normal coronary arteries and valvular thrombi. The fifth patient had a malignancy, and died one day after the onset of acute MI. Autopsy revealed multiple occlusive thrombi in the small intramural coronary arteries of the left ventricular wall supplied by segment 14, without any stenosis in the feeding vessel. Most infarcts were localized in the territory supplied by 1 or 2 of the 3 epicardial coronary arteries, and coincided with the clinically diagnosed infarct site. The infarct size ranged from 3%-26% of the left ventricular wall, and infarcts were generally localized to the inner third of the wall (67 +/- 20%). Histological examination of the four patients with acute MI revealed diffuse CBN (86 +/- 14% of the infarcted area) and/or hemorrhage.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1997

[Hemodynamically induced cerebral infarcts. Clinical significance of infarct pattern and angiomorphology].

Classification of brain infarcts based on the location, size and shape of parenchymal damage alone can be difficult and misleading. This is particularly true in subcortical infarctions and infarcts in so-called watershed areas between neighboring territories of the main hemispheric arteries. Pathogenetic mechanisms, signs and symptoms, lesion patterns in CT and MRI are discussed as well as angiomorphological conditions. Hemodynamically induced low-flow infarcts are rare and show typical, but not pathognomic lesion patterns on CT and MRI. Characteristic subcortical chainlike and confluent lesions are located in the supra- and paraventricular white matter, representing the core of a hemodynamically induced infarction. Definite diagnosis of low-flow infarcts requires information on the underlying complex vascular compromise of the extra- and intracranial arterial circulation. A noncompetent circle of Willis is the main predisposing condition in hemispheric low-flow infarcts even in severe occlusive disease of the internal carotid arteries.

Cerebral Infarction↗
PubMed2006

Present treatment of acute myocardial infarction in patients over 75 years--data from the Berlin Myocardial Infarction Registry (BHIR).

AIMS: Guidelines issued by European and German cardiology societies clearly define procedures for treatment of acute myocardial infarction (AMI). These guidelines, however, are based on clinical studies in which older patients are underrepresented. Older patients, on the other hand, represent a large and growing portion of the infarction population. It was our goal in the present paper to analyse the present treatment of AMI patients over 75 years of age in the city of Berlin, Germany, with data gained from the Berlin Myocardial Infarction Registry (BHIR). METHODS: We prospectively collected data from 5079 patients (3311 men and 1768 women, mean age 65.6) with acute myocardial infarction who were treated in 25 hospitals in Berlin during the period 1999-2003. 1319 patients (25.9%) were older than 75 (mean age 82.5 years). RESULTS: Overall hospital mortality rate was 11.6%. In patients over 75, this rate was 23.9%; among the younger infarction population, it was 7.3%. In contrast to the younger AMI patients, the majority of those over 75 were female (62.5 vs 25.1% for the younger) and demonstrated a significantly higher frequency of all prognostically meaningful comorbidities (heart failure 14.4% vs. 3.5%; renal failure 11.5 vs 3.9%; diabetes 37.3 vs 24.3%). Clinical signs of severe infarction, moreover, were more common among the aged patients (pulmonary congestion 45.4 vs 19.7%; left bundle branch block 12.7 vs 3.6%). Pre-hospital time was prolonged (2.8 vs 2 h) and guideline-recommended therapy was applied significantly less frequently to AMI patients over 75 (reperfusion therapy 39.8 vs 71.7%, beta-blockers 62.8 vs 78.3%, statins 26.5 vs 45.5%). Multivariate analysis revealed the following factors to be independent predictors of hospital mortality in patients over 75: age (OR 1.05 per year), acute heart failure (OR 2.39), pre-hospital resuscitation (OR 10.6), cardiogenic shock (OR 2.73), pre-hospital delay >12 h (OR 1.68), and ST elevation in the first ECG (OR 2.09). Independent predictors of a favourable hospital course were as follows: admission to a hospital >600 beds (OR 0.64), reperfusion therapy (OR 0.63), early betablocker treatment (OR 0.46), and early application of ACE inhibitors (OR 0.48). CONCLUSION: Infarction patients over 75 have a very high hospital complication and mortality rate. They are typically treated with delay, and with less adherence to relevant guidelines than are younger patients. Reperfusion therapy, early administration of beta-blockers and ACE inhibitors, as well as admission to large medical centres are all factors that contribute to a favourable prognosis of high-aged AMI patients.

Adrenergic beta-Antagonists↗
PubMed2002

Increased expression of dermatopontin mRNA in the infarct zone of experimentally induced myocardial infarction in rats: comparison with decorin and type I collagen mRNAs.

OBJECTIVES: Dermatopontin, a 22 kDa extracellular matrix (ECM) protein, has been shown to interact with other ECM components, especially decorin, and to regulate ECM formation. We examined dermatopontin mRNA expression in the myocardial infarct zone. METHODS: The cDNA encoding the rat dermatopontin was cloned by RT-PCR based on screening results from the Expressed Sequence Tag database. The dermatopontin mRNA expression was examined in the infarct zone after experimentally induced myocardial infarction in rats by the methods of Northern blotting and in situ hybridization. The expression of dermatopontin mRNA was compared to that of decorin and type I collagen mRNAs. RESULTS: The isolated clone contained a 609 bp cDNA insert containing a complete open reading frame encoding 202 amino acids. The rat dermatopontin cDNA showed high homology to human and mouse counterparts (>96 %). Northern blotting demonstrated that dermatopontin mRNA expression did not markedly increase on day 2, but was increased on days 7, 14 and 28 by 2.4-, 4.1- and 4.2-fold, respectively, compared to that in preligation hearts. Dermatopontin mRNA expression was regulated almost in parallel with decorin mRNA expression. In situ hybridization demonstrated mRNA signals for dermatopontin in macrophages and spindle-shaped mesenchymal cells (fibroblasts and myofibroblasts) located in the infarct interior zone around infarcted necrotic tissue on day 7. Coexpression of dermatopontin mRNA with decorin and type I collagen mRNAs was observed in spindle-shaped mesenchymal cells. CONCLUSIONS: The present results demonstrated the time-dependent increase in the expression of dermatopontin mRNA in parallel with that of decorin mRNA in the infarct zone. Coexpression of dermatopontin mRNA with decorin and type I collagen mRNAs suggests that dermatopontin plays a role in ECM (fibrillar collagen matrix) reformation in the infarct along with decorin and type I collagen.

Animals↗
PubMed2004

No effect of stem cell mobilization with GM-CSF on infarct size and left ventricular function in experimental acute myocardial infarction.

OBJECTIVES: To evaluate the effect of bone marrow pluripotent stem cell mobilization with granulocyte-monocyte colony stimulating factor (GMCSF) on infarct size and left ventricular function, in the setting of acute myocardial infarction, with a protocol easily applicable in clinical practice. METHODS: Ten pigs underwent left thoracotomy and left anterior descending coronary artery occlusion for 1 h, followed by reperfusion. After 50 min of arterial occlusion, the animals were randomly divided between treatment with placebo (Group 1) and subcutaneous GM-CSF (Group 2). The thoracotomy was closed and the animals recovered. In Group 2, GM-CSF, 20 microg/kg, was administered daily, 5 days/week, for 3 weeks. Echocardiograms were obtained at 5 and 28 days after acute myocardial infarction. At 30 days, infarct size, expressed as a percentage of the whole left ventricular mass, was measured. RESULTS: The white blood cell count increased from 13000 +/- 3338/ microl to 28700 +/- 4916/ microl (p = 0.001) in the GM-CSF-treated group. Infarct size was 7.8 +/- 6.1% in Group 1 vs 7.5 +/- 7.7% in Group 2 (ns). Similarly, no significant difference was observed between the 2 study groups in any of the echocardiographic measurements made at 28 days. CONCLUSIONS: Subcutaneous GMCSF administered during the early post acute myocardial infarction period neither decreased infarct size nor improved left ventricular function. Other protocols for mobilization of stem cells and their concentration in the injured area should be developed to combine efficacy and clinical applicability.

Animals↗
PubMed2005

Infarct size reduction and attenuation of global left ventricular remodeling with the CorCap cardiac support device following acute myocardial infarction in sheep.

BACKGROUND: Whether mechanical restraint of the left ventricle (LV) can influence remodeling following myocardial infarction (MI) remains poorly understood. The following discussion details three studies examining the effects of surgically placing a cardiac support device (CSD) over the entire epicardial surface, on infarct expansion, global cardiac function and myocyte geometry and function post-MI. METHODS: The effects of passive constraint on infarct expansion and global cardiac function/myocardial energetics were investigated in 10 sheep (5 MI only; 5 MI + CSD) using pressure-volume analysis and magnetic resonance imaging (MRI). Additionally, 11 sheep (5 MI only; 6 MI + CSD) were used to study the effects of passive restraint on myocyte geometry and function post-MI, with 10 additional uninstrumented sheep serving as controls. Baseline data was collected followed by the creation of an anterior infarct. 1 week post-infarct the animals underwent a second set of data collection studies followed by placement of the CSD in the experimental groups. Additional data was collected at 2 and 3 months post-MI. The animals in the myocyte function group underwent additional studies immediately following the 3 month time point. RESULTS: Infarct expansion was diminished as a result of the CSD. At 1 week post-MI the akinetic area was similar in both groups. At the terminal time-point, the akinetic area in the control group was similar to the 1-week time-point whereas, in the CSD group, the area of akinesis decreased (P = 0.001). A comparison of the two groups at the terminal time-point demonstrates a significantly diminished area of akinesis in the CSD group (P = 0.004). The relative area of akinesis followed a similar pattern. The CSD group also exhibited a decrease in end-diastolic volume (control 110.3 +/- 19.8 mL vs. CSD 67.6 +/- 4.7 mL, P = .006) and an improved ejection fraction (control 15.5% +/- 5.7% vs. CSD 29.46% +/- 4.42%, P = .008) relative to the control group. Myocardial energetics were also enhanced in the CSD group as evidenced by significant improvements in potential energy (control 2,015 +/- 503 mL x mm Hg/beat vs. CSD 885 +/- 220 mL x Hg/beat, P = .006), efficiency (control 39.4% +/- 13.6% vs. CSD 59.8% +/- 8.5%, P = .044), and oxygen consumption (control 0.072 +/- 0.013 mL O(2)/beat vs. CSD 0.052 +/- 0.007 mL O(2)/beat, P = .034). Isolated LV myocyte shortening velocity was reduced by 35% from control values (P < 0.05) in both MI groups. LV myocyte beta-adrenergic response was reduced with MI, but normalized in the MI + CSD group. Relative collagen content was increased and matrix metalloproteinase-9 was decreased within the MI border region of the CSD group. CONCLUSIONS: The CorCap cardiac support device retarded infarct expansion, improved global and regional cardiac function and beneficially modified LV and myocyte remodeling post-MI. These findings provide evidence that non-pharmacological strategies can interrupt adverse LV remodeling post-MI.

Animals↗
PubMed1987

Percutaneous transluminal coronary angioplasty in patients with prior myocardial infarction: angioplasty at a distance from the prior infarct zone.

Patients undergoing coronary angioplasty who have had a prior transmural myocardial infarction in the distribution of a contralateral coronary artery are considered a high-risk group because of potentially severe left ventricular dysfunction if an ischemic complication occurs. The purpose of this study was to evaluate the safety and efficacy of coronary angioplasty in 28 patients with prior myocardial infarction remote from the artery undergoing dilatation. Prior myocardial infarction was defined by the presence of pathologic Q waves on ECG or segmental akinesis on ventriculography. Angioplasty was successful in 30 of 33 lesions (91%) and in 25 of 28 patients (89%). Mean stenosis diameter was reduced from 91% +/- 7% to 28% +/- 16%; mean translesional gradient after angioplasty was 6 +/- 5 mm Hg. No patient developed severe hemodynamic deterioration from transient coronary occlusion during balloon inflation or from an acute ischemic complication. Three patients underwent coronary artery bypass surgery after unsuccessful angioplasty. There were no new Q wave infarctions or deaths. The results of coronary angioplasty in patients with prior infarction were compared with those of 203 patients without prior remote infarction. Primary success and occurrence of major complications were comparable in both groups. At a mean follow-up of 12 +/- 6 months, 18 of the 25 patients (72%) who underwent initially successful dilatation have remained symptom free with angioplasty alone. Therefore, coronary angioplasty is a suitable therapeutic procedure in carefully selected patients with angina pectoris and prior myocardial infarction at a distance from the site of angioplasty.

Adult↗
PubMed1988

Recurrent ischemia in the zone of prior myocardial infarction: results of coronary angioplasty of the infarct-related artery.

We studied the efficacy of coronary angioplasty (PTCA) of the infarct-related artery in 54 patients with recurrent myocardial ischemia in the zone of prior infarction. Our patients had recurrent ischemia 10 +/- 7 days after infarction, with 75% experiencing rest angina and 15% having evidence of reinfarction. Angiography of the infarct-related artery demonstrated a critical stenosis in 35 of 54, a subtotal occlusion in 5 of 54, and a total occlusion in 14 of 54. PTCA was successful in 94% of critical stenoses, 80% of subtotal occlusions, but in only 50% of total occlusions. Complications related to PTCA included a 3.7% rate of emergency surgery, but no deaths or infarctions. During the clinical follow-up period of 11 +/- 7 months, there was one reinfarction and no deaths. Although 27% of our 44 patients with a successful initial PTCA required a second revascularization procedure for recurrent angina, 40 patients (91%) remained symptomatically improved with angioplasty alone (including successful repeat PTCA in eight patients). We conclude that PTCA of the infarct-related artery is beneficial for selected patients with recurrent ischemia in the zone of prior infarction.

Adult↗
PubMed1990

Heparin and infarct coronary artery patency after streptokinase in acute myocardial infarction.

Anticoagulant therapy is frequently used after thrombolytic agents in the treatment of acute myocardial infarction (AMI) although it is unclear that such therapy will prevent subsequent infarct vessel reocclusion. The role of duration of heparin therapy in maintaining infarct artery patency was studied retrospectively in 53 consecutive AMI patients who received streptokinase therapy and underwent coronary angiography acutely and at 14 +/- 1 days. Of the 39 patients with initial infarct vessel patency, patency at follow-up angiography was observed in 100% (22 of 22) of those who received greater than or equal to 4 days of intravenous heparin but in only 59% (10 of 17) of those patients who received less than 4 days of heparin (p less than 0.05). Of the 14 patients not initially recanalized after streptokinase, patent infarct-related arteries at follow-up angiography were found in 3 of 8 (38%) treated with greater than or equal to 4 days of heparin therapy but in none of the 6 patients treated for less than 4 days (difference not significant). No significant difference in hemorrhagic complications was noted between the short- and long-term heparin treatment groups. Thus, greater than or equal to 4 days of intravenous heparin therapy after successful streptokinase therapy in AMI is more effective in maintaining short-term infarct vessel patency than a shorter duration of therapy and it may maintain the short-term patency of the infarct vessel in those patients who later spontaneously recanalize.

Angiography↗
PubMed1990

Influence of anterograde flow in the infarct artery on the incidence of late potentials after acute myocardial infarction.

In patients after myocardial infarction, survival is influenced by the presence or absence of anterograde flow in the infarct artery, and late potentials on signal-averaged electrocardiography identify those at risk for tachyarrhythmias and sudden death. To assess the frequency of late potentials in survivors of first infarction, coronary arteriography and signal-averaged electrocardiography were performed in 109 subjects (64 men, 45 women, aged 30 to 77 years), 49 with (group I) and 60 without (group II) anterograde flow in the infarct artery. The groups were similar in age, sex, infarct artery, severity of coronary artery disease and left ventricular function. However, only 4 (8%) of group I had late potentials, whereas 24 (40%) of group II had late potentials (p less than 0.001). Thus, anterograde flow in the infarct artery after myocardial infarction is associated with a low incidence of late potentials on signal-averaged electrocardiography, whereas the absence of anterograde flow is more often associated with late potentials.

Adult↗
PubMed1981

Effect of PGE1, PGE2 and PGI2 on ventricular arrhythmias during myocardial infarction in conscious dogs: relation to infarct size.

The relation between the effect of vasodilator prostaglandins on ventricular arrhythmias during myocardial infarction and infarct size was studied in conscious dogs. Two infarct-limiting drugs, nitroglycerin and ibuprofen, were also studied for comparison. Infusions were given between 20 and 380 minutes after occlusion of the left circumflex coronary artery: intravenously for saline (N = 27), ibuprofen (N = 14), and nitroglycerin (N = 14); left atrially for PGE1 (N = 11), PGE2 (N = 12) and PGI2 (N = 18). Doses of prostaglandins and nitroglycerin were adjusted to decrease mean arterial pressure by 5%. Pathologic infarct size was measured 2 days post-occlusion. During the infusion period, ventricular fibrillation (VF) deaths were nil with PGI2 (p less than 0.05) and nitroglycerin (p less than 0.1), ventricular premature beats (VPB's) were less (p less than 0.01) with PGI2, PGE2 and nitroglycerin, and collateral blood flow (microspheres) increased with PGE1, PGI2 and nitroglycerin but did not change with saline, PGE2 and ibuprofen. Infarct size, as percent of left ventricle or occluded bed, was less (p less than 0.05) with PGE1, PGI2, nitroglycerin and ibuprofen but similar with PGE2 and saline. Thus, PGE2 diminished VPB's despite no effect on flow or infarct size. In contrast, both PGE1 and PGI2 diminished VPB's, increased flow and decreased infarct size, but PGI2 also reduced VF mortality.

Alprostadil↗
PubMed1989

Early treatment with intravenous metoprolol for suspected acute myocardial infarction: a phase IV United States trial. Phase IV Metoprolol in Myocardial Infarction Study Group.

Recent randomized clinical trials have shown that total mortality and cardiovascular mortality are reduced by the early intravenous administration of beta-blockers to patients suspected of suffering from acute myocardial infarction. These trials were conducted on patients meeting strict entry criteria. In order to assess this therapy when applied to a broader range of myocardial infarction patients, we performed a Phase IV study of metoprolol in acute myocardial infarction. The study was designed to test whether early (less than 8 hours from onset of chest pain) intervention by practicing physicians with open label intravenous metoprolol for cases of suspected acute myocardial infarction achieved mortality results similar to those obtained in large randomized clinical trials. We studied 3824 patients treated by 741 physicians representing a broad spectrum of clinical practice in the United States. Seventy-two percent of the patients entered into the study had confirmed myocardial infarction (39% anterior, 39% inferior, 22% other locations) and 85% of all individuals treated tolerated the full intravenous dose of 15 mg of metoprolol. The 15 day total mortality and cardiovascular mortality rates were 4.9% and 4.5%; 90 day mortality rates were 6.9 and 5.9%. Patients with anterior infarctions had a significantly greater cumulative mortality rate than patients with other types of infarctions. Marked bradycardia (heart rate less than 45 beats per minute) in the first 8 hours post treatment occurred in 4.7% cases and hypotension (systolic blood pressure less than 90 mm Hg) occurred in 9.8% of cases. When compared with the results of the Göteborg and MIAMI trials of metoprolol, it appears that there is no appreciable increase in mortality or morbidity when metoprolol is used in the community practice of acute coronary care.

Adult↗
PubMed1993

Influence of infarct-related artery patency on the indexes of parasympathetic activity and prevalence of late potentials in survivors of acute myocardial infarction.

OBJECTIVES: The purpose of this study was to determine whether infarct-related coronary artery patency influences myocardial electrical stability as measured by the prevalence of late potentials or heart rate variability. BACKGROUND: Several studies have suggested that loss of vagal activity is associated with an increased incidence of arrhythmic death after myocardial infarction. METHODS: A short-duration, high resolution electrocardiogram (ECG) was performed before hospital discharge in 175 patients with a first myocardial infarction. Seventy-three patients received thrombolytic therapy. All patients underwent coronary angiography. Coronary occlusion was defined as minimal or no anterograde flow. Eighty-eight patients (50.3%) had an occluded infarct-related artery. Sixty-two healthy subjects served as control subjects to determine the normal range of heart rate variability. RESULTS: Comparison between the control group and patients without patency of the infarct-related artery in the time domain and spectral analyses revealed in the latter patients a reduced heart rate variability (p < 0.0001) and a lower power spectrum density in both the 0.05- to 0.15-Hz band (p < 0.0001) and the 0.15- to 0.35-Hz band (p < 0.0001). The heart rate variability in patients with late potentials was lower than in those with a normal signal-averaged ECG. Those patients with spontaneous or thrombolysis-induced reperfusion have less occurrence of late potentials and higher parasympathetic activity than do patients with a closed artery. CONCLUSIONS: This study suggests that the patency of the infarct-related artery determines both the absence of late potentials and the preservation of vagal tone and may explain the reduction in mortality induced by thrombolytic therapy in myocardial infarction.

Adult↗
PubMed1993

Effect of thrombolysis on acute mitral regurgitation during evolving myocardial infarction. Experience from the Thrombolysis in Myocardial Infarction (TIMI) Trial.

OBJECTIVES: This study was undertaken to determine whether early successful thrombolysis can reverse infarct-associated mitral valve dysfunction. BACKGROUND: Mitral regurgitation is a common complication of acute myocardial infarction and has been shown to adversely affect both short- and long-term prognosis. Although anecdotal reports have suggested that reperfusion of the infarct-related artery may restore normal function to the mitral valve, this theory has not been subjected to formal investigation. METHODS: Patients with total or partial obstruction of the infarct-related artery received intravenous thrombolytic therapy with either streptokinase or recombinant tissue-type plasminogen activator within 7 h of symptom onset (mean 4.8 h) as part of the Thrombolysis in Myocardial Infarction (TIMI) Phase I trial. Repeat coronary angiography assessed arterial patency at 90 min and 10 days after attempted reperfusion. The presence and severity of mitral regurgitation were determined by contrast ventriculography both before thrombolysis and before hospital discharge. RESULTS: Overall, 21 (16%) of the 132 study patients exhibited mitral regurgitation on either their initial or their predischarge ventriculogram. The proportion of infarct-related arteries found to be patent (TIMI flow grade 2 or 3) was statistically similar in patients with and without mitral regurgitation during each angiographic evaluation period (initial, 90 min and 10 days). Although coronary artery perfusion increased overall during sequential measurement (mean TIMI grade was 0.4 +/- 0.6 initially, 1.5 +/- 1.3 at 90 min and 2.2 +/- 1.0 at 10 days), the pattern of reperfusion observed could not predict an increase or decrease in regurgitant severity (p = NS). Early mitral regurgitation resolved in 57% of patients by 10 days, but this resolution appeared independent of the presence or absence of improved coronary perfusion (60% vs. 50%). The development of new regurgitation during the recovery period (6%) was also unrelated to improved perfusion (7% vs. 4%). CONCLUSIONS: Acute mitral regurgitation developing during myocardial infarction shows frequent changes in its presence or severity during the 1st 10 days, appears independent of coronary artery patency both early and late after thrombolysis and cannot be reliably treated by improving arterial perfusion with thrombolytic agents.

Acute Disease↗
PubMed1994

Influence of residual perfusion within the infarct zone on the natural history of left ventricular dysfunction after acute myocardial infarction: a myocardial contrast echocardiographic study.

OBJECTIVES: This study used myocardial contrast echocardiography to investigate the extent of residual perfusion within the infarct zone in a select group of patients with recently reperfused myocardial infarction and evaluated its influence on the ultimate infarct size. BACKGROUND: Limited information is available on the status of myocardial perfusion within postischemic dysfunctional segments at predischarge and on its influence on late regional and global functional recovery. METHODS: Twenty patients with acute myocardial infarction were selected for the study. Patients met the following inclusion criteria: 1) single-vessel coronary artery disease; 2) patency of infarct-related artery with persistent postischemic dysfunctional segments at predischarge; 3) stable clinical condition up to 6 months after hospital discharge. All selected patients underwent coronary angiography and myocardial contrast echocardiography before hospital discharge and repeated the echocardiographic examination 6 months later. Patients were grouped according to the pattern of contrast enhancement in predischarge dysfunctional segments. RESULTS: In nine patients (group I), the length of segments showing abnormal contraction coincided with that of the contrast defect segments. In the remaining 11 patients (group II), postischemic dysfunctional segments were partly or completely reperfused. There was no difference between the two groups in asynergic segment length at predischarge (7.3 +/- 2.5 vs. 7.2 +/- 4.3 cm, p = NS). At follow-up study, asynergic segment length was significantly reduced in group II patients, whereas no changes were observed in group I patients (from 7.2 +/- 4.3 to 4.7 +/- 3.7 cm, p < 0.005; and from 7.3 +/- 2.5 to 7.5 +/- 2.9 cm, p = NS, respectively). CONCLUSIONS: Among patients with a predischarge patent infarct-related artery, further improvement in regional and global function may be expected during follow-up when residual perfusion in the infarct zone is present.

Adult↗
PubMed2004

Quantitative myocardial contrast echocardiography for prediction of thrombolysis in myocardial infarction flow in acute myocardial infarction.

Clinical evaluation of arterial patency in acute ST-elevation myocardial infarction (STEMI) is unreliable. We sought to identify infarction and predict infarct-related artery patency measured by the Thrombolysis In Myocardial Infarction (TIMI) score with qualitative and quantitative intravenous myocardial contrast echocardiography (MCE). Thirty-four patients with suspected STEMI underwent MCE before emergency angiography and planned angioplasty. MCE was performed with harmonic imaging and variable triggering intervals during intravenous administration of Optison. Myocardial perfusion was quantified offline, fitting an exponential function to contrast intensity at various pulsing intervals. Plateau myocardial contrast intensity (A), rate of rise (beta), and myocardial flow (Q = A x beta) were assessed in 6 segments. Qualitative assessment of perfusion defects was sensitive for the diagnosis of infarction (sensitivity 93%) and did not differ between anterior and inferior infarctions. However, qualitative assessment had only moderate specificity (50%), and perfusion defects were unrelated to TIMI flow. In patients with STEMI, quantitatively derived myocardial blood flow Q (A x beta) was significantly lower in territories subtended by an artery with impaired (TIMI 0 to 2) flow than those territories supplied by a reperfused artery with TIMI 3 flow (10.2 +/- 9.1 vs 44.3 +/- 50.4, p = 0.03). Quantitative flow was also lower in segments with impaired flow in the subtending artery compared with "normal" patients with TIMI 3 flow (42.8 +/- 36.6, p = 0.006) and all segments with TIMI 3 flow (35.3 +/- 32.9, p = 0.018). An receiver-operator characteristic curve derived cut-off Q value of <11.3, representing impaired myocardial flow, was 73% sensitive and 67% specific for TIMI <3 flow at angiography. Thus, qualitative MCE identifies patients with STEMI but provides no information regarding infarct-related artery patency, whereas quantitative MCE can predict impaired flow in patients with acute STEMI.

Coronary Angiography↗
PubMed2004

Differential prognostic significance of peri-infarction versus remote myocardial ischemia on stress technetium-99m sestamibi tomography in patients with healed myocardial infarction.

Peri-infarction and remote myocardial ischemia involve different myocardial substrates, but their differential clinical implications have not been previously studied. We assessed the differential prognostic significance of peri-infarction and remote ischemia during long-term follow-up in patients with healed myocardial infarction. We studied 345 patients (59 +/- 12 years old; 282 men) with previous myocardial infarction who demonstrated reversible perfusion abnormalities on exercise or dobutamine stress technetium-99m sestamibi tomography. Follow-up events for 5.5 +/- 2.6 years were 60 deaths (17%; 40 cardiac deaths) and 25 reinfarctions (7%). Reversible perfusion abnormalities were detected in the remote region in 129 patients (37%), the peri-infarction region in 142 patients (41%), and in both regions in 74 patients (21%). The annual rates of cardiac death in these groups were 1.2%, 2.8%, and 2.9%, respectively (p <0.01). The annual rates of reinfarction were 1%, 1.5%, and 0.9%, respectively (p = NS). In a multivariate analysis model, independent predictors of cardiac death were history of heart failure (risk ratio [RR] 2.8, 95% confidence interval [95% CI] 1.2 to 7), diabetes mellitus (RR 4.1, 95% CI 1.9 to 8.9), summed score at rest (RR 1.4, 95% CI 1.1 to 3.1), and peri-infarction ischemia (RR 2.6, 95% CI 1.1 to 6.1). Predictors of reinfarction were age (RR 1.03, 95% CI 1.01 to 1.07) and diabetes mellitus (RR 3.3, 95% CI 1.2 to 9.1). Peri-infarction ischemia assessed by stress technetium-99m sestamibi tomography is associated with a greater risk of cardiac death than is remote ischemia. The risk of reinfarction is not related to the location of ischemia.

Aged↗
PubMed2005

Effects of reperfusion obtained two to six months after acute myocardial infarction on myocardial electrical stabilization in patients with an occluded infarct-related coronary artery.

To assess the changes in electrical stability markers in patients with previous myocardial infarction after very late reopening of the infarct-related artery, we studied QT dispersion, corrected-QT dispersion, and late potentials before and 1, 3, and 6 months after an attempt at late percutaneous coronary intervention (PCI) in 31 consecutive patients with single-vessel disease (infarct-related artery occlusion or subocclusion) diagnosed > or = 4 weeks after the ST-elevation myocardial infarction. Patients underwent PCI 3.9 +/- 2 months after ST-elevation myocardial infarction. PCI was successful in 24 patients (group A) and unsuccessful in 7 (group B). The 2 groups were similar in clinical and angiographic characteristics, as well as the prevalence of basal late potentials, average QT dispersion, and corrected-QT dispersion. One month after PCI, the successful reperfusion group had a significant 67% decrease in the prevalence of late potentials and average QT dispersion and corrected QT dispersion (51 +/- 9 vs 72 +/- 11 ms, p <0.00001, and 51 +/- 10 vs 76 +/- 15 ms, p <0.00001, respectively). These benefits remained stable at 3 and 6 months after PCI. Conversely, the unsuccessful group did not show any improvement in electrical stability markers after PCI failed. Thus, reperfusion obtained very late after ST-elevation myocardial infarction confers significant electrical stabilization that may contribute to a better outcome in patients with patent infarct-related arteries.

Aged↗