Sequelae Of Acute Myocardial Infarction Research Articles

Prognostic impact of lean diabetes mellitus on aortic stenosis

Abstract Background Obesity and type 2 diabetes mellitus (DM) has traditionally been thought to coexist. Lean DM is a distinct condition defined by body mass index (BMI) < 25, associated with elevated insulin resistance, rapid beta-cell failure, absence of ketosis and malnutrition. Lean DM has been linked to poor cardiovascular outcomes, but remains an understudied entity in valvular heart disease. Purpose This study aims to demonstrate the prognostic implications of lean DM on aortic stenosis (AS). Methods Between 2011 to 2021, 700 consecutive patients with index echocardiographic diagnoses of aortic stenosis were stratified into 4 groups, namely lean (BMI < 25) DM, lean non-DM, obese (BMI > 25) DM, and obese non-DM. Demographics, co-morbidities, echocardiographic findings and clinical outcomes were collected. Clinical outcomes were compared using Kaplan-Meier curves and a multivariate Cox regression model was constructed. Results 396 (56.6%) patients were female, and 435 (62.1%) patients were of Chinese ethnicity. 279 (39.9%) patients had DM, of whom 155 (55.6%) patients had lean DM. The mean BMI in the lean group was 21.4 ± 2.4 kg/m² compared to 29.5 ± 4.9 kg/m² in the obese group. Irregardless of BMI, higher proportions of DM patients were on baseline antiplatelets and statins compared to non-DM patients. Echocardiographically, obese DM had smaller indexed left ventricular volumes and mass - left ventricular end diastolic volume index (LVEDVi) (65.7 ± 21.7 ml/m² vs. 70.8 ± 23.6 ml/m², p = 0.002) and left ventricular mass index (LVMi) (115.7 ± 31.9 g/m² vs. 116.3 ± 36.5 g/m², p = 0.401) compared to lean DM respectively. Obese DM was associated with more cardiovascular risk factors compared to lean DM in terms of hypertension (91.9%, n = 114 vs. 89.0%, n = 138, p < 0.001), hyperlipidaemia (82.3%, n = 102 vs. 73.5%, n = 114, p < 0.001) and chronic kidney disease (50.8%, n = 62 vs. 45.5%, n = 70, p < 0.001). On the contrary, lean DM was associated with more cardiovascular sequelae of acute myocardial infarction (36.8%, n = 57 vs. 24.2%, n = 30, p < 0.001) compared to obese DM. AS patients with lean DM experienced the highest significant all-cause mortality (71%, n = 110 in lean DM vs. 58.9%, n = 73 in obese DM vs. 49.1%, n = 86 in obese non-DM vs. 65%, n = 160 in lean non-DM, p < 0.001) compared to all other groups. On the contrary, AS patients with lean DM had the lowest heart failure incidence (17.4%, n = 27 in lean DM vs. 23.4%, n = 29 in obese DM vs. 33.1%, n = 58 in obese non-DM vs. 23.2%, n = 57 in lean non-DM, p = 0.009). On multivariate analyses adjusted for age, comorbidities, and echocardiographic parameters, lean DM was an independent predictor of worse all-cause mortality in AS patients (HR 1.60, CI: 1.19 - 2.16, p = 0.010). Conclusion Lean DM in AS patients was associated with worse all-cause mortality. Lean DM was a prognostic marker of all-cause mortality in patients with AS.Figure 1

Prevalence and clinical outcomes of acute myocardial infarction in patients presenting with major trauma

BackgroundThe occurrence and sequelae of acute myocardial infarction (AMI) in major trauma patients is underexplored across both trauma and cardiology specialties. Coronary reperfusion greatly reduces the risk of significant morbidity and mortality in AMI. However, in patients presenting with significant injuries, concurrent AMI presents a competing management priority given the increase in risk of bleeding with standard anticoagulation and antiplatelet therapy, which may be contraindicated. This study aimed to evaluate the epidemiology and clinical outcomes associated with AMI in a contemporary major trauma cohort. MethodsThis study used data from the Victorian State Trauma Registry (VSTR). All adult patients with major trauma from 1 January 2013 to 31 December 2022 were included. Patients that died prior to hospital arrival were excluded. AMI was identified by ICD-10-AM diagnosis codes recorded against the first hospital admission. Clinical outcomes included in-hospital mortality, length of stay, and discharge destination. Results28,928 patients were identified over the 10-year study period. AMI occurred in 401 patients (1.4 %). AMI patients were older, had more comorbidities and were more frequently on anticoagulation or antiplatelet therapy. Low impact fall was the most common trauma mechanism in AMI patients. Patients with AMI experienced longer hospital stays (12 [7–20] versus 7 [4–12] days, p < 0.001) and higher rates of in-hospital mortality (adjusted RR 1.45, 95 % CI 1.25–1.65). ConclusionAMI in the setting of major trauma occurs in an older, more comorbid, and vulnerable group of patients. AMI is associated with an increased risk of in-hospital mortality and prolonged hospital stay in the setting of major trauma, underscoring the importance of identifying and treating major trauma associated AMI in a timely and effective manner.

Long-term survival after surgical treatment for post-infarction mechanical complications: results from the Caution study.

Mechanical complications (MCs) are rare but potentially fatal sequelae of acute myocardial infarction (AMI). Surgery, though challenging, is considered the treatment of choice. The authors sought to study early and long-term results of patients undergoing surgical treatment for post-AMI MCs. Patients undergone surgical treatment for post-infarction MCs between 2001 through 2019 in 27 centers worldwide were retrieved from the database of CAUTION study. In-hospital and long-term mortality were the primary outcomes. Cox proportional hazards regression models were used to determine independent factors associated with overall mortality. The study included 720 patients. The median age was 70.0 [62.0-77.0] years, with a male predominance (64.6%). The most common MC encountered was ventricular septal rupture (VSR) (59.4%). Cardiogenic shock was seen on presentation in 56.1% of patients. In-hospital mortality rate was 37.4%; in more than 50% of cases, the cause of death was low cardiac output syndrome (LCOS). Late mortality occurred in 133 patients, with a median follow-up of 4.4 [1.0-8.6] years. Overall survival at 1, 5 and 10 years was 54.0%, 48.1% and 41.0%, respectively. Older age (p<0.001) and postoperative LCOS (p<0.001) were independent predictors of overall mortality. For hospital survivors, 10-year survival was 65.7% and was significant higher for patients with VSR than those with papillary muscle rupture (long-rank P=0.022). Contemporary data from a multicenter cohort study show that surgical treatment for post-AMI MCs continues to be associated with high in-hospital mortality rates. However, long-term survival in patients surviving the immediate postoperative period is encouraging.Trial registration number: NCT03848429.

Sex differences in trends and outcomes of acute myocardial infarction with mechanical complications in the United States

ABSTRACT Background Mechanical complications (MC) are rare but significant sequelae of acute myocardial infarction (AMI). Current data on sex differences in AMI with MC is limited. Methods We queried the National Inpatient Sample database to identify adult patients with the primary diagnosis of AMI and MC. The main outcome of interest was sex difference in-hospital mortality. Secondary outcomes were sex differences in the incidence of acute kidney injury (AKI), major bleeding, use of inotropes, permanent pacemaker implantation (PPMI), performance of percutaneous coronary intervention (PCI), coronary artery bypass grafting (CABG), surgery (VSD repair and MV surgery), pericardiocentesis, use of mechanical circulatory support (MCS), ischemic stroke, and mechanical ventilation. Results Among AMI-MC cohort, in-hospital mortality was higher among females compared to males (41.24% vs 28.13%: aOR 1.39. 95% CI 1.079–1.798; p = 0.01). Among those who had VSD, females also had higher in-hospital mortality compared to males (56.7% vs 43.1%: aOR 1.74, 95% CI 1.12–2.69; p = 0.01). Females were less likely to receive CABG compared to males (12.03% vs 20%: aOR 0.49 95% CI 0.345–0.690; p < 0.001). Conclusion Despite the decreasing trend in AMI admission, females had higher risk of MC and associated mortality. Significant sex disparities still exist in AMI treatment.

Pericarditis and Post-cardiac Injury Syndrome as a Sequelae of Acute Myocardial Infarction.

Pericarditis secondary to acute myocardial infarction (AMI) is known to develop either immediately or after a latent period of few months. Due to varied presentation and timing, its diagnosis and treatment can be challenging. This article reviews underlying mechanisms and the role of cardiac imaging in investigating and managing this condition. Timely diagnosis of pericarditis after AMI is important to prevent potential progression to complicated pericarditis. Clinical suspicion warrants initial investigation with serum inflammatory levels, electrocardiogram, and echocardiography. When findings are inconclusive, cardiac magnetic resonance imaging and computerized tomography can provide additional diagnostic information. Pericarditis after AMI is a treatable condition. Clinicians should maintain a high suspicion in this era of revascularization and develop a strategic plan for timely diagnosis and management.

TNF‐alpha Produces Endothelial Dysfunction in Diabetes

Diabetes is leading risk factor for ischemic heart disease, and recent evidence suggests that inflammation is involved in the pathophysiological sequelae of acute myocardial infarction. We hypothesized that the inflammatory cytokine, tumor necrosis factor alpha (TNF) produces endothelial dysfunction in Type II diabetes. To test this, endothelium-dependent (acetylcholine, ACh) and –independent vasodilation (sodium nitroprusside, SNP) of isolated, pressurized (60 cmH2O) coronary arterioles (50–100 μm) from genetically modified mice with Type II diabetes (db/db) and the lean control heterozygotes (Db/db) were determined. In Db/db mice, SNP and ACh induced dose-dependent vasodilation, and dilation to ACh was blocked by the NOS inhibitor NG-monomethyl-L-arginine (L-NMMA, 10 μM) (P<0.05). In db/db, dilation to ACh was blunted compared to Db/db (P<0.05), but SNP produced comparable dilation. Plasma concentration of TNF was significantly increased in db/db mice vs Db/db, 6.89±0.3 vs 1.14±0.2, respectively (P<0.05). Immunostaining result show that TNF in mouse heart is localized predominantly in vascular smooth muscle cells rather than in cardiac muscle and endothelial cells. Neutralizing antibodies to TNF (72 hr treatment; 0.625 mg/kg, i.p.) restored NO-mediated coronary arteriolar dilation in db/db mice. In conclusion, an increase in circulating and/or the local vascular TNF in Type II diabetes induces endothelial dysfunction in db/db mice.

Metabolic Therapy for Heart Disease: Impact of Trimetazidine

Coronary artery disease remains the major contributor to the development of heart failure. Despite the massive efforts targeted toward preventative therapy and life style changes, the incidence of coronary artery disease continues to be high, shows little or no signs of abatement, and remains the leading health economic burden in developed countries and, for that matter, worldwide. There is no doubt that the aggressive use of thrombolytic therapy and primary coronary angioplasty has had a major impact on limiting the sequelae of acute myocardial infarction. There is also little doubt that routine coronary revascularization through coronary artery bypass surgery or coronary angioplasty with attendant coronary stent deployment has had a positive impact, albeit transient, on limiting symptoms of coronary artery disease. Despite all of these successes of the twentieth century, however, chronic stable angina pectoris remains a major clinical problem that must be dealt with by cardiologists, internists and primary care physicians alike as we move into the next millenium. Many of the patients that present with stable angina pectoris are not candidates for further revascularization, or, in this the age of rationed health care, even if eligible, must “stand in line” to have the procedure performed. Needless to say that most, if not all, of these patients are candidates for the development of congestive heart failure (CHF), truly the disease of the next millenium. The myocardium depends on oxygen to support high energy phosphate production by oxidative phosphorylation. The latter is the only metabolic process that can generate sufficient chemical energy to fuel the continuous needs of the contractile machinery of the heart. Accordingly, when the amount of oxygen delivered to the myocardium is insufficient to meet the requirements for mitochondrial respiration, the production of high energy phosphates falls and lactate, the end product of anaerobic glycolysis, starts to accumulate. The interruption of oxygen supply to the myocardium or ischemia, regardless of etiology, leads to the clinical symptom of angina pectoris. Ischemia can be defined as an imbalance between the supply of oxygenated blood to the myocardium and the oxygen requirements of the myocardium. When the supply of oxygen cannot meet the demands, as is the case when coronary artery disease is present, contractile function diminishes along with clinical manifestation of anginal pain. The latter the result of stimulation of cardiac sensory afferent nerve fibers by “noxious stimuli” produced in the myocardium. The cardiac sensory afferents nerves are stimulated by a rise in interstitial adenosine and K+, both of which increase when oxygen delivery and aerobic ATP synthesis are reduced [1]. Electrocardiographically, ischemia is reflected through ST-segment elevation or depression on the electrocardiogram with the latter believed to reflect delayed repolarization in the ischemic zone, and has recently been attributed to KATP channels [2], which presumably open in response to the fall in ATP. Taken together, both angina and ST-segment changes during ischemia are arguably the result of a failure to regenerate ATP, and as such, are of metabolic origin.

Sequelae of Acute Myocardial Infarction Regarding Cardiac Structure and Function and Their Prognostic Significance as Assessed by Magnetic Resonance Imaging

Sequelae of Acute Myocardial Infarction Regarding Cardiac Structure and Function and Their Prognostic Significance as Assessed by Magnetic Resonance Imaging

Sequelae of acute myocardial infarction regarding cardiac structure and function and their prognostic significance as assessed by magnetic resonance imaging

Because of its high spatial resolution and tissue contrast, magnetic resonance imaging (MRI) was used to assess cardiac structure and function in a large population of patients with acute myocardial infarction (AMI). One hundred and ten patients were studied by MRI 6.1 +/- 2.2 days after AMI. Infarct size (IS), persistent microvascular obstruction (PMO), left and right ventricular (LV/RV) volumes, and functions were measured. The same MRI measurements were repeated in 89 patients after a mean follow-up period of 225 +/- 92 days. IS was 11.9 +/- 7.3% of total LV muscle mass. PMO was detected in 51/110 (46.4%) patients and comprised 15.6 +/- 8.5% of IS and 2.8 +/- 2.3% of LV muscle mass. Papillary muscle infarct was seen in 26%, RV infarction in 16%, pericarditis in 40%, and pericardial effusion in 66% of the patients. During follow-up, there were 16 major adverse cardiac events (MACE) including seven deaths. IS, PMO, and amount of transmural infarction were predictive for LV adverse remodelling defined as > 20% increase in LV end-diastolic volume. Multivariable analysis revealed LV end-diastolic volume, LV ejection fraction, and PMO as significant predictors for the occurrence of MACE. MRI is a highly sensitive and reliable tool to detect morphologic and functional sequelae of AMI providing baseline MRI parameters with relevant predictive power for LV adverse remodelling and occurrence of MACE.

The prognostic significance of microvascular obstruction after myocardial infarction as defined by cardiovascular magnetic resonance

This editorial refers to ‘Sequelae of acute myocardial infarction regarding cardiac structure and function and their prognostic significance as assessed by magnetic resonance imaging’† by V. Hombach et al. , on page 549 Cardiac magnetic resonance imaging (CMR) has evolved into an important imaging tool in the assessment of patients with myocardial infarction (MI), with or without reperfusion. CMR is a gold standard technique for measuring left ventricular volumes and global function.1 The technique of delayed contrast enhancement has been carefully validated in animal markers as a measure of infarct size.2 The presence of hypo-enhanced regions at the core of hyper-enhanced infarctions is a marker of microvascular obstruction (MO)3 and a predictor of lack of functional recovery in the infarct zone4 and poor cardiovascular outcome in the patient post-MI.5 The paper by Hombach et al. 6 is the largest report to date of these CMR techniques used in sequential fashion in patients with acute MI and thus is quite instructive regarding prognostic factors derived from CMR. These authors studied 110 patients at a mean of day 6 after acute MI, which is a relatively late initial time point as patients currently are typically discharged before day 6. Of the original 110 patients, 89 returned for follow-up imaging at an average of ∼9 months after MI. The remainder died ( n =7), refused follow-up ( n =11), or had … *Corresponding author. Tel: 434 243 6060; fax: 434 982 1618. E-mail address : ckramer{at}virginia.edu

The Pathology of Acute Myocardial infarction: Definition, Location, Pathogenesis, Effects of Reperfusion, Complications, and Sequelae

This article reviews the definition, locations, and pathogenesis of acute myocardial infarction and provides a review of the pathology of acute reperfusion therapy. Various complications and sequelae of acute myocardial infarction are also surveyed.

Clot-Selective Coronary Thrombolysis with Tissue-Type Plasminogen Activator

Coronary thrombolysis, an intervention that can abort the sequelae of acute myocardial infarction, was accomplished within 10 minutes in dogs by intravenous administration of clot-selective, tissue-type plasminogen activator. In addition to inducing clot lysis, this promising fibrinolytic agent restored intermediary metabolism and nutritional myocardial blood flow, detectable noninvasively with positron tomography, without inducing a systemic fibrinolytic state.

A prosthetic myocardium for repair of localized defects of the left ventricle: Concept and hemodynamic feasibility

As an approach to the treatment of patients with large but circumscribed akinetic or dyskinetic regions in the left ventricular myocardium as sequelae of acute myocardial infarction, excision of the defect and implantation of a mechanical functional equivalent of myocardium is suggested. Experimental investigation of this technique is described. Hemodynamic data from a series of dog experiments indicate that activation of the prosthetic myocardium after excision of the left ventricle is followed by improvement in various hemodynamic parametres of interest. Although substantial experimental work must be completed and difficult bioengineering problems solved, preliminary results have encouraged us to continue our investigations of the prosthetic myocardium. An imposing array of treatment methods is now available to the clinician who must deal with the sequelae of acute myocardial infarction. Selecting from pharmacologic, electrophysiologic, and surgical approaches the physician can in many instances design a treatment plan precisely tailored to the clinical problem. Large left ventricular aneurysms and their functional equivalents of ventricular dyskinesis or hypokinesis continue, however, to represent a class of problems in which established techniques have been less than satisfactory. Surgical excision with closure of the defect is regarded as effective for small aneurysms, but such procedures may so compromise cardiac output in patients with large ones as to be unacceptable. Unfortunately, it is just the latter group in which medical palliation is least likely to be effective in managing congestibe failure, angina, and other pathophysiologic manifestations. A relatively unusual approach derived from in-series techniques of mechanical assistance to the failing circulation (1) offers the theoretical possibility of a treatment tailored to the problem of a large ventricular aneurysm. Experimental investigation of this technique in the Surgical Research Laboratory at the Sinai Hospital of Detroit has progressed to the point that a report of our experiences to date may be of interest.

Reduction of ischemic injury by nitroglycerin during acute myocardial infarction.

ARRHYTHMIAS and cardiac failure are two of the major, potentially lethal sequelae of acute myocardial infarction. Although measures used to treat arrhythmias are usually considered separately from those used to treat myocardial failure, it is clear that arrhythmias and myocardial failure share a common precipitating mechanism —severe ischemic injury (as defined by a reduction in oxygen delivery to the myocardial cell resulting initially in aberrations of biochemical, electrophysiologic and mechanical function and, if unrelieved, ultimately in cell death). Moreover, in some cases of acute myocardial infarction complicated by left ventricular failure and ventricular arrhythmias, the temporal sequence of events suggests . . .

THE SELECTIVE USE OF ANTICOAGULANTS IN ACUTE MYOCARDIAL INFARCTION BASED ON INITIAL PROGNOSIS

Excerpt Reliable evidence accumulated in the last 10 years has indicated that anticoagulants are of decided value in the prevention and treatment of thromboembolic diseases. Beginning with Wright's...

The treatment of postmyocardial infarction shoulder-hand syndrome with local hydrocortisone.

In a series of 18 consecutive cases of the shoulder-hand syndrome, a causalgic state which is one of the sequelae of acute myocardial infarction, favorable results were obtained by infections of hydrocortisone in trigger areas about the shoulder girdle.

Complications and sequelae of acute myocardial infarction.

The prognosis of the immediate illness in acute myocardial infarction is determined principally by the size of the infarcted area and by whether certain complications develop. In patients who recover, ultimate longevity and the degree of functional rehabilitation attained depend to a large extent on whether certain sequelae occur. The purpose of this paper is to review the most important of the complications and sequelae of acute myocardial infarction, with particular reference to their clinical features and to the prevention or treatment of those for which prophylactic or therapeutic measures are available. COMPLICATIONS The principal complications of acute myocardial infarction are shock, acute left ventricular failure, congestive heart failure, abnormalities of cardiac rhythm, thromboembolism, rupture of the ventricle, perforation of the interventricular septum, and rupture of a papillary muscle. Each of these conditions will be considered briefly. Shock. —A shock-like state of mild to severe degree occurs in 50% or