Setting Of Myocardial Infarction Research Articles

Native cardiac reserve predicts survival in acute post infarction heart failure in mice

Cardiac reserve can be used to predict survival and outcome in patients with heart failure. The aim of this study was to investigate if native cardiac reserve could predict survival after myocardial infarction (MI) in mice.MethodWe investigated 27 healthy C57Bl6 mice (♂10–12 weeks old) with echocardiography using a high-frequency 15-MHz linear transducer. Investigations were performed both at rest and after pharmacological stress induced by dobutamine (1 μg/g body weight i.p.). The day after the echocardiography examination, a large MI was induced by ligation of the left anterior descending (LAD) coronary artery for evaluation of mortality rate.ResultsTwo weeks after induction of MI, 7 mice were alive (26%). Evaluation of the difference between the surviving and deceased animals showed that the survivors had a better native ability to increase systolic performance (ΔLVESd -1.86 vs -1.28mm p = 0.02) upon dobutamine challenge, resulting in a better cardiac reserve (ΔFS 37 vs 25% p = 0.02 and ΔCO 0.27 vs -0.10 ml/min p = 0.02) and a better chronotropic reserve (ΔR-R interval -68 vs -19 ms p < 0.01). A positive relationship was found between ability to survive and both cardiac (p < 0.05) and chronotropic reserve (p < 0.05) when the mice were divided into three groups: survivors, surviving < 7 days, and surviving < 1 day.ConclusionWe conclude that before MI induction the surviving animals had a better cardiac function compared with the deceased. This indicates that native cardiac and chronotropic reserve may be an important determinant and predictor of survival in the setting of large MI and post-infarction heart failure.

Effect of Anemia and Red Blood Cell Transfusion in Acute Myocardial Infarction.

Background: The optimal hemoglobin (Hb) in the setting of acute myocardial infarction (MI) is unknown. Anemia reduces the oxygen carrying capacity of blood and may theoretically exacerbate ischemia increasing myocardial injury. The benefit of transfusion to correct anemia in acute coronary syndromes is also controversial. The goal of this study was to determine the optimal Hb in the setting of acute MI and whether transfusion reduces myocardial injury and improves outcome.Experimental design: Ninety-two male Sprague-Dawley rats (170–190g) were divided into 8 groups: 1: Normal Hb, sham operation; 2: Normal Hb, MI; 3: Hb 80–90g/L, sham; 4: Hb 80–90g/L, MI; 5: Hb 70–80g/L, sham; 6: Hb 70–80g/L, MI; 7: Hb 80–90g/L, MI with transfusion to 100g/L; 8: Hb 80–90g/L, MI with transfusion to 120g/L. To determine the effect of blood transfusion, fresh blood was immediately transfused following MI. Induction of myocardial infarction was preformed by left coronary artery ligation. Sham-operated rats underwent the same surgical procedure without ligation. At 24 hours post-MI, rats were re-anaesthetized and hemodynamic measurements preformed. Area at risk and infarct size was measured by Evans blue and triphenyltetrazolium chloride, respectively.Results: In the normal Hb group (140–150g/L), survival following sham or MI surgery was 100%. Reduction of Hb to 80–90 and 70–80g/L significantly decreased survival post-MI to 42% and 47%, respectively. Survival was significantly improved after transfusion of fresh blood to raise the hemoglobin from 80–90g/L to 100g/L (P<0.05). However, there was no improvement in survival when Hb was raised by transfusion to 120g/L (P=NS). Twenty-four hours post-MI, the ischemic to non-ischemic left ventricle (LV) weight ratios were not significantly different between any groups indicating similar areas of myocardial ischemia among all groups (P=NS). However, the infarct size to area at risk ratios were significantly increased in both 70–80g/L and 80–90g/L groups compared to the normal Hb group (P<0.05). Transfusion from Hb 80–90g/L to 100g/L significantly decreased infarct size compared to the Hb 80–90g/L group (P<0.05). However, transfusion to Hb 120g/L resulted in a significantly larger infarct size compared to the Hb 100g/L transfused group (P<0.05). Cardiac function was determined at 24 hours post-MI. Heart rate, MAP, LVSP and LVEDP were not significantly different among all groups but anemic groups 80–90 and 70–80g/L showed a significant decrease in LV +dP/dtmax and −dP/dtmin in both sham and MI rats (P<0.01) with the most significant decrease noted in MI rats compared to sham operated rats (P<0.05). Blood transfusion post-MI from a Hb 80–90 to 100g/L significantly improved LV +dP/dtmax (P<0.05). Transfusion to Hb 120g/L did not result in any further improvement in cardiac function.Conclusions: In the setting of acute MI, anemia increased mortality and infarct size compared to non-anemic controls. At 24 hours post-MI, anemia also impaired cardiac function. Transfusion of anemic animals up to a Hb of 100g/L with fresh RBCs reduced mortality and infarct size and improved cardiac function. However, transfusion to a Hb of 120g/L did not demonstrate any additional benefit and was associated with larger infarcts.

Drug-Eluting Stent Update 2007

Randomized trials have largely demonstrated that percutaneous coronary intervention (PCI) with sirolimus-eluting (SES) and paclitaxel-eluting stents (PES) results in a significant reduction in the occurrence of angiographic restenosis and revascularization compared with bare metal stents (BMS).1–4 The benefit of drug-eluting stents (DES) also has been confirmed in “real-world” scenarios. In this setting, when the analysis was focused on high-risk patient and lesion subgroups, a benefit still existed despite the presence of restenosis.5–7 These expanded indications do not yet cover many other types of complex lesions for which only registries or randomized trials, not yet published, are available so far (Tables 1 through 7⇓⇓⇓⇓⇓⇓). This topic is discussed in detail in this review. An important clarification is that the lack of proof is most probably due to the difficulty in performing randomized trials in high-risk groups using BMS as controls. It will be no surprise to find that the field in which DES perform best compared with BMS is likely to be complex lesions and patients8 (Figure 1). View this table: TABLE 1. DES in Unprotected Left Main Stenosis View this table: TABLE 2. DES in Bifurcation Lesions View this table: TABLE 3. DES in Chronic Total Occlusions View this table: TABLE 4. DES in Small-Vessel Disease and Long Lesions View this table: TABLE 5. DES in SVGs View this table: TABLE 6. DES in Acute MI View this table: TABLE 7. DES in Multivessel Disease Figure 1. Lesion complexity and stent performance in the BMS and DES eras. Adapted from Edelman et al.8 Current American Heart Association/American College of Cardiology (AHA/ACC) and European Society of Cardiology (ESC) guidelines consider the presence of a stenosis in the unprotected left main coronary artery (LMCA) a class IIa or IIb indication, respectively, for PCI if coronary artery bypass grafting (CABG) is not a viable option.9,10 Moreover, according to the AHA/ACC 2005 guidelines, in …

Cardiovascular events and re-stenosis following administration of G-CSF in acute myocardial infarction: systematic review and meta-analysis

Background: Because of the recently published results of the MAGIC study there is confusion as to whether administration of granulocyte-colony stimulating factor (G-CSF) after acute myocardial infarction (MI) should be...

Late ventricular remodeling in non-reperfused acute myocardial infarction in humans is predicted by angiotensin II type 1 receptor density on blood platelets

Background Ventricular remodeling after myocardial infarction (MI) is largely dependent on renin–angiotensin system activity, which is determined by angiotensin II concentration and angiotensin II type 1 receptor (AT 1R) density in target tissues. We have recently shown that AT 1R density in the acute phase of MI determines post-MI ventricular remodeling at discharge (8 days). The aim of this study was to test whether this correlation is retained in a longer follow-up (6 months), in the same group of patients. Methods In 48 patients with first acute MI who did not undergo reperfusion therapy, angiotensin AT 1R density on blood platelets (a presumable marker of cardiovascular AT 1R density) was assessed 13 ± 5 h after the onset of MI, using radioligand binding assay. Echocardiographic indices of left ventricular function and dimensions were used as measures of ventricular remodeling. Results 6 months after the infarction patients who at baseline had AT 1R density above median ( N = 17) as compared to those with AT 1R density below median ( N = 20) had higher left ventricular end-systolic volume index (LVESVI, 41.3 ± 2.7 vs. 33.2 ± 2.3) and lower ejection fraction (LVEF 48.1 ± 1.8 vs. 54.7 ± 2.0). Moreover LVESVI positively and LVEF negatively correlated with AT 1R density although the strength of these correlations was weaker than at discharge. Infarct size as reflected by a single troponin T measurement and post-MI therapy did not differ between high- and low-AT 1R groups: over 85% patients received ACE-inhibitor, β-blocker and statin. Conclusions High AT 1R density on blood platelets (a presumable marker of cardiovascular AT 1R density) drawn in the acute phase of MI predicts poorer left ventricular systolic function in 6-month follow up. This suggests that modern therapy offers suboptimal blockade of renin–angiotensin system activity in the setting of MI.

Hyperaemic microvascular resistance is not increased in viable myocardium after chronic myocardial infarction

The present study compared microvascular resistance (MR) of viable myocardium in infarct areas with those in reference areas in patients with chronic myocardial infarction (MI). In 27 patients, MR (ratio distal coronary pressure and flow) of reference and viable infarct areas was calculated at baseline and during hyperaemia. H2 15O positron emission tomography (PET) was used to provide myocardial blood flow measurements. In infarct regions, H2 15O PET solely measures flow in viable myocardium, excluding flow in scar tissue. Distal coronary pressure was measured with a pressure wire in the infarct-related and reference artery. The average time between PET study and infarction was 3.3+/-4.4 years. Mean hyperaemic distal coronary pressure was significantly lower in the infarct-related artery. MR varied considerably between patients and was significantly higher in infarct areas at baseline (135+/-38 vs. 118+/-29 mmHg mL min/mL; P<0.05), but not during hyperaemia (39+/-18 vs. 35+/-11 mmHg mL min/mL). The correlation between MR in infarct and reference areas was significant. To determine MR, distal coronary pressure measurements should be used. Hyperaemic MR in viable myocardium within the infarcted area is not higher when compared with the reference area. This supports the application of the established fractional flow reserve cut-off value in the setting of chronic MI.

Myocardial infarct size measurement in the mouse chronic infarction model: comparison of area- and length-based approaches

Efficacy of potential treatments for myocardial infarction (MI) is commonly assessed by histological measurement of infarct size in rodent models. In experiments involving an acute MI setting, measurement of the infarcted area in tissue sections of the left ventricle is a standard approach to determine infarct size. This approach has also been used in the chronic infarct setting to measure infarct area several weeks post-MI. We tested the hypothesis that, because wall thinning is known to occur in the chronic setting, the area measurement approach would be less appropriate. We compared infarct measurements in tissue sections based on 1) infarct area, 2) epicardial and endocardial infarct arc lengths, and 3) midline infarct arc length. Infarct sizes from all three measurement approaches correlated significantly with left ventricular ejection fraction and wall motion abnormality. However, the infarct size values derived from the area measurement approach were significantly smaller than those from the other two measurement approaches, and the range of values obtained was compressed 0.4-fold. The midline method allowed detection of the expected size differences between infarcts of variable severity resulting from proximal vs. distal ligation of the coronary artery. Segmental infarct size was correlated with segmental wall motion abnormality. We conclude that both area- and length-based measurements can be used to determine relative infarct size over a wide range of severity, although the area-based measurements are substantially more compressed due to wall thinning, and that the estimation of infarct midlines is a simple, reliable approach to infarct size assessment.

Myocardial infarction: contemporary management strategies

Myocardial infarction (MI) is a common clinical diagnosis, associated with significant morbidity and mortality, not only in the short term, but also years following the index event. A more complete understanding of the pathophysiology of MI has ushered the era of multipronged treatment approach, with a combination of goal-directed revascularization, a broad adjunctive pharmacological therapy and aggressive secondary prevention measures. The goals of this article are to review the basic pathophysiological processes, which lead up to a clinical diagnosis of MI, to highlight the essential elements of clinical presentation and to summarize the evidence for comprehensive therapy. Emphasis has been placed on the choice of primary reperfusion therapy for ST-elevation MI, on risk-stratification of patients with non-ST elevation MI, and on rationale behind the selection of anti-ischaemic and antithrombotic therapy. Finally, evidence-based approach to secondary prevention is outlined.

Transplanted human umbilical cord blood mononuclear cells improve left ventricular function through angiogenesis in myocardial infarction

Human umbilical cord blood contains an abundance of immature stem/progenitor cells, which may participate in the repair of hearts that have been damaged by myocardial infarction (MI). This study aimed to evaluate the effects of human umbilical cord blood mononuclear cells (hUCBC) transplantation on cardiac function and left ventricular remodeling in rat model of MI. Forty-five male Wistar rats were randomized into three groups: MI or control group (n = 15), MI plus cell transplantation (n = 15), and sham group (n = 15). Acute myocardial infarction (AMI) was established by ligating the left anterior descending artery, thereafter, hUCBC were implanted into the marginal area of infarcted myocardium. In MI/control group, DMEM was injected instead of hUCBC following the same protocol. Left ventricular function assessment was carried out by echocardiography and invasive hemodynamic measurements one month post MI. All rats were sacrificed for histological and immunochemical examinations. The transplanted hUCBC survived and engaged in the process of myocardial repair in the host heart. Echocardiography demonstrated that left ventricular function improved significantly in the rats that underwent cell transplantation. Hemodynamic studies found a significantly decreased left ventricular end-diastolic pressure (LVEDP) [(21.08 +/- 8.10) mmHg vs (30.82 +/- 9.59) mmHg, P < 0.05], increase in +dp/dt(max) [(4.29 +/- 1.27) mmHg/ms vs (3.24 +/- 0.75) mmHg/ms, P < 0.05), and increase in -dp/dt(max) [(3.71 +/- 0.79) mmHg/ms vs (3.00 +/- 0.49) mmHg/ms, P < 0.05] among MI group with hUCBC transplantation when compared with MI/control group. Masson's trichrome staining revealed that the collagen density in the left ventricle was significantly lower in rats of transplantation group than that in the MI control groups [(6.33 +/- 2.69)% vs (11.10 +/- 3.75)%, P < 0.01]. Based on immunostaining of alpha-actin, the numbers of microvessels were significantly (P < 0.01) increased at the boundary of infarction site. Similarly higher mRNA expression of vascular endothelial growth factor (VEGF) 164 and VEGF188 were found at 7- and 28-day post cell transplantation in MI group with hUCBC transplantation when compared with MI/control group. Transplanted hUCBC can survive in host myocardium without immunorejection, significantly improve left ventricular remodeling after AMI and promote a higher level of angiogenesis in the infarct zones. All these factors beneficially affect cardiac repair in the setting of MI. Therefore human umbilical cord blood may be potential source for cell-based therapy for AMI.

Prognostic implications of PR-segment depression in inferior leads in acute inferior myocardial infarction

Concurrent atrial ischemia is usually overlooked in acute myocardial infarction (MI) due to its subtle electrocardiographic (ECG) changes, lack of clear-cut clinical picture, and prognostic significance. PR-segment depression in the inferior leads is a simplified ECG sign for detecting possible underlying atrial ischemia. The purpose of this study was to document the incidence, clinical characteristics, and prognostic implications of this ECG sign in the setting of acute inferior MI. Demographics, clinical characteristics, and outcomes of 463 consecutive patients presenting with acute inferior MI were reviewed. The in-hospital ECG was examined by two independent reviewers. The results were then compared between those with and without ECG sign. Profound PR-segment depression > or = 1.2 mm in inferior leads was found in 9 of 463 (1.9%) patients. Patients with atrial ischemia tended to present earlier (2.4 +/- 2.6 vs. 7.0 +/- 8.2 h, p = 0.000) and had a higher frequency of first-degree atrioventricular block (77.8 vs. 30.6%, p = 0.028) and supraventricular arrhythmias (55.5 vs. 20.2%, p = 0.022). Of greater importance, it was significantly associated with an increased rate of cardiac free-wall rupture (33.3 vs. 2.0%, p = 0.001) and in-hospital mortality (44.4 vs. 11.7%, p = 0.015). Profound PR-segment depression > or = 1.2 mm in inferior leads was associated with a complicated hospital course and poor short-term outcome in acute inferior MI. These patients were at high risk for the development of atrioventricular block, supraventricular arrhythmias, and cardiac free-wall rupture.

239. Histological Measurement of Myocardial Infarct Area Does Not Provide a Sensitive Assessment of Infarct Size in a Mouse Chronic Infarct Model

Assessment of severity of a myocardial infarction (MI) is an important measure of success after experimental delivery of potentially therapeutic genes or cells in rodent MI models. In experiments involving an acute MI setting, histological measurement of the area of the infarcted region in tissue sections of the left ventricle (LV) is a standard assessment of |[ldquo]|infarct size.|[rdquo]| This approach is also used by numerous investigators in a chronic infarct setting, taking infarct area measurements several weeks post-MI. However, we hypothesized that wall thinning due to remodeling of a transmural infarct would invalidate the correlation between a severe infarct and a large infarct scar area measurement, reducing the legitimacy of this approach in a chronic setting. To address this issue, we assessed left ventricular ejection fraction (LVEF; cardiac systolic function) in 8 infarcted mouse hearts and ranked them according to increasing severity. Tissue sections were collected approximately every 300 uM from apex to base and were stained with Masson's trichrome to visualize the infarct scar. The scar was measured in each section by a blinded investigator using several strategies, the numbers obtained were combined to express infarct size as percentage of total LV volume, and the values were compared to the functional measurements for each heart. Our measurement strategies consisted of calculation of the ratio of (1) summed infarct areas to summed LV myocardial areas (Area Measurement: AM), (2) summed epicardial and endocardial infarct arc lengths to summed epicardial and endocardial LV circumferences (Length Measurement: LM), and (3) summed midline infarct arc lengths to summed midline LV circumferences (Midline Length Measurement: MLM). Linear correlation analyses showed that infarct size from all three measurement approaches correlated significantly with LVEF (r=0.87, p<0.01 for each method) and wall motion score index (r=0.97-0.98, p<0.01 for each). However, the infarct size calculated using AM was significantly smaller than those using the other measurements (average of values obtained for all hearts studied: AM 10.83|[plusmn]|6.53% vs. LM 26.72|[plusmn]|19.04%, MLM 26.08|[plusmn]|20.94%, p<0.01), and the range of values obtained was compressed 0.4-fold, substantially compromising the accuracy of this approach. We conclude that while wall thinning did not invalidate the use of area-based infarct size measurements, it underestimated the extent of the infarct and substantially reduced the sensitivity of this measure compared to measurements based on infarct arc lengths. We further conclude that the estimation of myocardial and infarct midlines provided comparable accuracy to the more cumbersome tracing of epicardial and endocardial lengths and circumferences. These findings demonstrate that the ratio of summed infarct midlines to summed LV midlines is significantly better than infarct area measurements as an assessment of infarct size in cell or gene therapy studies in chronic rodent MI models.

Periprocedural Cardiac Enzyme Elevation Predicts Adverse Outcomes

Extensive clinical investigation throughout the 1990s validated periprocedural myonecrosis as a powerful predictor of adverse outcomes, so it is surprising that this remains a contentious point. Originally derided as “enzyme leaks” or “myocardial infarctlets,” periprocedural myocardial infarction (MI) has now been definitively linked in large data sets to long-term adverse outcomes, most notably mortality. It is not, however, always directly contributory or causative. For example, a large creatine kinase (CK) elevation caused by closure of a major side branch resulting in chest pain and development of new Q waves is obviously undesirable and causally related to the interventional procedure. Alternatively, even small, asymptomatic CK elevations have been clearly associated with worse long-term outcome, and although this may in part be causally related to the procedure, it is more likely that the relationship is caused by the underlying predisposing factors that led to the periprocedural MI, such as arterial inflammation predilecting to the occurrence of embolization or to a large degree of atheroma burden leading to more myonecrosis. Under these circumstances, it is likely that the heightened inflammatory state and the diffuse disease that is present are the real causative factors for worse long-term outcomes. Recently, aspirin resistance has been demonstrated to predict periprocedural myonecrosis. Thus, both through direct causation and also as an epiphenomenon, embolization and attendant periprocedural myonecrosis are associated with short, intermediate, and long-term adverse outcomes (Table 1). This review details this evolution in thought. View this table: TABLE 1. Mechanisms Behind Periprocedural Myonecrosis Periprocedural myonecrosis is a frequent occurrence in percutaneous coronary intervention (PCI). CK or CK myocardial band (CK-MB) elevation occurs in ≈25% of patients undergoing PCI. With the advent of sensitive troponin measurements, it is clear that at least 50% of patients undergoing PCI have postprocedural troponin elevation, reflecting the frequency with which embolization occurs. However, troponin offers …

Incidence, predictors, and outcomes of high-degree atrioventricular block complicating acute myocardial infarction treated with thrombolytic therapy

In the fibrinolytic era, several studies have suggested that the rate of atrioventricular block (AVB) in the setting of acute myocardial infarction (MI) is high and is associated with increased short-term mortality. We sought to delineate predictors of AVB and determine long-term mortality of patients developing AVB in the setting of ST-segment elevation MI (STEMI) treated with thrombolytic therapy. We combined data on patients from 4 similar studies of STEMI. We identified independent predictors of AVB and compared the 6-month and 1-year mortality rates of patients with AVB (5251) to the rates of patients without AVB (70 742). The incidence of AVB was 6.9%. Significant independent predictors of AVB included inferior MI, older age, worse Killip class at presentation, female sex, enrollment in the United States, current smoking, hypertension, and diabetes. Adjusted mortality was significantly higher in patients with AVB than in patients without AVB within 30 days (OR 3.2, 95% CI 2.7-3.7), 6 months (OR 1.6, 95% CI 1.5-1.8), and 1 year (OR 1.5, 95% CI 1.3-1.6). For patients with AVB and inferior MI, mortality odds ratios (ORs) were 2.2 (95% CI 1.7-2.7), 2.6 (95% CI 2.4-2.9), and 2.4 (95% CI 2.2-2.6) within 30 days, 6 months, and 1 year, respectively. For patients with AVB and anterior MI, mortality ORs were 3.0 (95% CI 2.2-4.1), 3.5 (95% CI 3.1-3.8), and 3.3 (95% CI 3.0-3.7) within 30 days, 6 months, and 1 year, respectively. In the thrombolytic era, AVB in the setting of STEMI is common and associated with higher mortality. Future studies should focus on determining therapies that are effective at reducing mortality rates in such patients.

Coronary and myocardial angiography: angiographic assessment of both epicardial and myocardial perfusion.

Angiographic assessment of epicardial coronary artery blood flow has played a pivotal role in our understanding of the “time-dependent open artery hypothesis” and in the evaluation of reperfusion strategies over the past 2 decades.1–8 It has become increasingly apparent, however, that clinical outcomes are not only associated with angiographic flow in the epicardial artery, but also with angiographic flow in the myocardium.9–13 To this end, the goal of reperfusion therapies has shifted to include reperfusion downstream at the level of capillary bed, and it might be more appropriate that the hypothesis now be termed “the time dependent open artery and open microvascular hypothesis.” The goal of this article is to review angiographic methods used to evaluate myocardial ischemia and infarction and to discuss the insights into the pathophysiology of acute coronary syndromes provided by these angiographic indexes of coronary artery blood flow and myocardial perfusion. For nearly 2 decades now, the Thrombolysis In Myocardial Infarction (TIMI) flow grade classification scheme has been successfully used to assess coronary blood flow in acute coronary syndromes1 (Table). It has been a valuable tool to compare angiographic outcomes following reperfusion, and the association of the TFGs with clinical outcomes (including mortality) has been well documented.2–8 The relationship between TFG and mortality does satisfy what some consider to be 3 criteria required to validate a surrogate end point for mortality, as follows: (1) There is an association between TIMI grade 3 flow and mortality, (2) an agent such as recombinant tissue plasminogen activator improves TIMI grade 3 flow by 22% over another agent such as streptokinase, and (3) the agent tissue plasminogen activator improves mortality 1.1% over streptokinase. View this table: Definitions of the TFG and the TMPG Systems On the basis of this relationship between TIMI flow and mortality observed in the GUSTO …

21 Growth hormone decreases ventricular arrhythmias in rats with acute postinfarct heart failure

Introduction: A growing body of evidence suggests a possible role for growth hormone (GH) in the treatment of congestive heart failure (CHF) and myocardial infarction (MI). Excess sympathetic activity (SA) is a key arrhythmogenic factor both in the setting of acute MI and during chronic CHE The aim of this study was to investigate interaction GH SA and the effects of GH treatment on ventricular arrhythmias in rats with postinfarct heart failure. Methods: Male rats weighing ~350 g were randomized into 3 groups. GH treated rats (n = 6) received 6mg/kg of human GH. The placebo group (n=10) received 1 ml of saline. Amiodarone treated rats (n=10) were injected with 25mg/kg and served as positive controls. All rats received a single injection 6 h prior to MI. MI was induced by ligation of the left coronary artery resulting in a large (~40%) anterolateral MI. ECG tracing and invasive hemodynamics were registered for 60 min post MI. At 60 rain or at the time of death 1 ml blood was drawn for analysis of catecholamines. Qualitative as well as quantitative variables of ventricular arrhythmias were analyzed according to the 10-point arrhythmia score. Results: The arrhythmia scores in the GH (3.8 41) and amiodarone (3.9 40.5) treated animals were significant lower than in the placebo group (5.9 40.5, p < 0.05). There was no significant difference in arrhythmia score between the GH and the amiodarone groups. GH treated rats had lower heart rate during postinfarct period.

Volumetric intravascular ultrasound evidence that distal embolization during acute infarct intervention contributes to inadequate myocardial perfusion grade

We studied 35 consecutive patients with myocardial infarction (MI) who were treated with direct infarct percutaneous coronary intervention (PCI) using standard angiographic (complete assessment of flow grade and blush grade) and pre- and post-PCI volumetric intravascular ultrasound analysis. Plaque reduction, which is evidence of distal embolization, contributes to inadequate tissue reperfusion in this lesion setting and supports the use of distal protection in the setting of an acute MI.

Early and long-term clinical outcomes associated with reinfarction following fibrinolytic administration in the thrombolysis in myocardial infarction trials

ObjectivesWe hypothesized that early recurrent myocardial infarction (MI) following fibrinolytic administration would be assessed with higher mortality at both 30 days and 2 years. BackgroundAlthough early recurrent MI after fibrinolytic therapy has been associated with increased early mortality in the acute MI setting, its relation to long-term mortality has not been fully explored. MethodsMortality data were ascertained in 20,101 patients enrolled in the Thrombolysis In Myocardial Infarction (TIMI) 4, 9, and 10B and Intravenous NPA for the Treatment of Infarcting Myocardium Early (InTIME-II) acute MI trials. ResultsThe frequency of symptomatic recurrent MI during the index hospitalization was 4.2% (836/20,101). Recurrent MI during the index hospital period was associated with increased 30-day mortality (16.4% [137/836] vs. 6.2% [1,188/19,260], p < 0.001). Likewise, recurrent MI was associated with a sustained increase in mortality up to two years, even after adjustments were made for covariates known to be associated with mortality and recurrent MI (hazard ratio 2.11, p < 0.001). However, this higher mortality at 2 years was due to an early divergence in mortality by 30 days and was not due to a significant increase in late mortality between 30 days and 2 years (4.38% [31/707] vs. 3.76% [685/18,206], p = NS). Percutaneous coronary intervention during the index hospitalization was associated with a lower rate of in-hospital recurrent MI (1.6% vs. 4.5%, p < 0.001) and lower two-year mortality (5.6% vs. 11.6%, p < 0.001). Performance of coronary artery bypass graft surgery was also associated with a lower recurrent rate of MI (0.7% vs. 4.3%, p < 0.001) and lower two-year mortality rate (7.95% vs. 10.6%, p = 0.0008). ConclusionsEarly recurrent MI is associated with increased mortality up to two years. However, most deaths occur early, and the risk of additional deaths between the index hospital period and two years was not significantly increased among patients with recurrent MI. Percutaneous coronary intervention during the index hospitalization was associated with a lower risk of recurrent MI and a lower risk of two-year mortality.

Preoperative cardiology consultation.

In a 1998 survey of New York metropolitan area anesthesiologists, surgeons, and cardiologists, the three specialties were in general agreement that important purposes of a cardiology consultation are to treat an inadequately treated cardiac condition before surgery (e.g., unstable angina or congestive heart failure [CHF]), to provide data to use in anesthesia management (e.g., ischemic threshold of tachycardia on stress test or left ventricular ejection fraction), and possibly to diagnose a medical condition before surgery (e.g., the cause of a new-onset atrial fibrillation). The yield of a cardiology consultation, in terms of new therapy or significant effect on patient management strategy prior to surgery, has, however, been reported to vary widely from 10% to more than 70%. The reasons why the consultation process often falls short of ideal are probably multifold, but may often originate from vague understanding of the consultation process. The physician initiating the consultation, whether an anesthesiologist or a surgeon, may not make it clear to the cardiologist why the consultation is being sought. In a retrospective review of 202 cardiology consultations at a university hospital, it was found that 108 just asked for an “evaluation,” 79 asked for a “clearance,” and 9 did not specifically request anything. Only six posed a specific question. As a result, the consultant often makes broadly inclusive, general remarks about perioperative management of the patient and may recommend preoperative diagnostic work-up that does not influence the patient’s outcome but prolongs the hospital stay. In this review are presented (1) the indications for cardiology consultations as implied in the American College of Cardiology–American Heart Association (ACC–AHA) guidelines on preoperative cardiac evaluation, and (2) suggestions on how the ACC–AHA guidelines may be critically applied to, and improve, the consultation process. Preoperative Cardiac Consultation Based on the ACC–AHA Guidelines The ACC–AHA guidelines on preoperative cardiac evaluation were published initially in 1996 and were also endorsed by the Society of Cardiovascular Anesthesiologists and the Society for Vascular Surgery. An updated version of the guidelines was published in 2002. The guidelines were based on the then-available literature as well as expert opinions from the disciplines of anesthesiology, cardiology, electrophysiology, vascular medicine, vascular surgery, and noninvasive cardiac testing. The guidelines provided an 8-step algorithm for stratifying the patient’s risks and triaging to either surgery or cardiac evaluation. The first three steps of the guidelines consider the urgency of the operation and the recency of cardiac evaluation and intervention. If the operation is not emergent and if there has not been recent cardiac evaluation and/or intervention with no significant interim changes, then the remainder of the guidelines are applied. Steps 4 through 7 deal with an assessment of the patient’s clinical predictors of cardiac risk, functional status, and the risk of the surgery proposed. Step 8, or noninvasive cardiac testing to further define the patient’s risk, is indicated (1) if the patient has a major clinical predictor, (2) if the patient has an intermediate clinical predictor and either has poor functional status or is undergoing a high-risk surgery, or (3) if the patient has poor functional status and is undergoing a high-risk surgery. As defined by the ACC–AHA, major clinical predictors are unstable coronary syndrome, decompensated congestive heart failure (CHF), significant arrhythmias, and severe valvular disease. Intermediate clinical predictors are mild angina pectoris, history of myocardial infarction (MI) or CHF, diabetes mellitus, and chronic renal failure with serum creatinine greater than 2 mg/dl. A high-risk surgery carries a greater than 5% perioperative risk of cardiac events such as MI, CHF, or death and is exemplified by emergent major operations, especially in the elderly, aortic, and other major vascular procedures, peripheral vascular bypass procedures, and anticipated prolonged surgical procedures associated with large fluid shifts and/or blood loss. An intermediate-risk surgery carries 1–5% perioperative risk of cardiac events and is exemplified by carotid endarterectomy, intraperitoneal and Director of Vascular Anesthesia, Department of Anesthesia & Critical Care, Beth Israel Deaconess Medical Center, and Associate Professor of Anaesthesia, Harvard Medical School.

Acute myocardial infarction in the elderly with diabetes

Objective: Diabetes mellitus (DM) has been associated with an elevated, short-term risk of death after myocardial infarction (MI). Among the studies of DM, however, few studies have included elderly subjects. The purpose of the present investigation was to determine if non-insulin-treated DM (NIRxDM) and insulin-treated DM (IRxDM) were associated with specific comorbid conditions, clinical findings on arrival, and MI characteristics, as well as a higher 30-day mortality rate in elderly patients with acute MI. Design: The study design was a retrospective medical record review and secondary data analysis of previously collected data from the Cooperative Cardiovascular Project. Setting: Study setting was Connecticut from June 1, 1992, through February 28, 1993. Patients: Subjects included the entire Medicare population (n = 2050), aged 65 years or older who were hospitalized for acute MI. Outcome Measures: Mortality rate at 30 days after MI was measured. Results: A history of DM was observed in 29% of the study population. DM status was associated with previous comorbid conditions, poorer functional status, higher body mass index, heart failure on arrival, non-Q-wave MI, and development of atrial fibrillation and oliguria during hospitalization. Patients with DM were less likely to have chest pain on arrival to the hospital. Diabetic status was not a significant predictor of short-term mortality; at 30 days after MI, 17% (n = 242) of the subjects without DM, 19% (n = 71) of those with NIRxDM, and 18% (n = 39) of the subjects with IRxDM died (P =.460). After adjustment for other prognostic factors, it was noted that MI characteristics present on hospital arrival predicted mortality at 30 days in both patients with NIRxDM and patients with IRxDM. Conclusions: The slightly, but not significantly, increased mortality risk in patients with DM should not minimize the importance of monitoring DM in the acute MI setting. Hospitalization for MI provides an opportunity to provide aggressive lipid and blood pressure management, optimize blood glucose, control heart failure, and institute other secondary preventive interventions in the elderly population with DM. (Heart Lung® 2002;31:327-39.)

Pause-dependent torsade de pointes following acute myocardial infarction: A variant of the acquired long QT syndrome

OBJECTIVESWe report on a previously unrecognized form of the long QT syndrome (QT interval prolongation andpause-dependent polymorphic ventricular tachycardia [VT]) entirely related to myocardial infarction (MI).BACKGROUNDPolymorphic VT in the setting of acute MI generally occurs during the hyperacute phase, is related to ischemia, and is not associated with QT prolongation. Although QT prolongation after MI is well described, typical pause-dependent polymorphic VT (torsade de pointes) secondary to uncomplicated MI was previously unknown.METHODSOf 434 consecutive admissions for acute MI, 8 patients had progressive QT prolongation that led to typical torsade de pointes. None of these patients had active ischemia or other known causes of QT prolongation. These patients were compared with 100 consecutive patients with uncomplicated MI who served as controls.RESULTSThe incidence of torsade de pointes following MI was 1.8% (95% confidence interval 0.8% to 3.6%). The QTc intervals of patients and controls were similar on admission. The QTc lengthened by day 2 in both groups, but more so in patients with torsade de pointes (from 470 ± 46 to 492 ± 57 ms [p < 0.05] and from 445 ± 58 to 558 ± 84 ms, respectively [p < 0.01]). Maximal QT prolongation and torsade de pointes occurred 3 to 11 days after infarction. Therapy included defibrillation, magnesium, lidocaine and beta-blockers. Three patients required rapid cardiac pacing. The long-term course was uneventful.CONCLUSIONSInfarct-related torsade de pointes is uncommon but potentially lethal. An acquired long QT syndrome should be considered in patients recovering from MI who experience polymorphic VT as specific therapeutic measures are mandatory.