Myocardial Infarction Failure Research Articles

Hiperglicemia como factor de riesgo de mortalidad hospitalaria en infarto de miocardio

Introduction: Myocardial infarction continues with high mortality rates, from 4.6% to 13.1%. There are predictive risk stratification models, such as the Grace Score, which does not include glycemia as a variable. Patients hospitalized for myocardial infarction with hyperglycemia on admission may have higher mortality, in ST elevated and non-elevated infarcts. Objectives: The objective of this review is to identify and systematize the evidence on hyperglycemia on admission as a biomarker of mortality and heart failure in acute myocardial infarction. Materials and Methods: The search was carried out in the MEDLINE database including the MeSH terms hyperglycemia and hospital mortality or heart failure in myocardial infarction, selecting 12 articles. Results: Hospital mortality was calculated in 11 articles, in 9 of them a significant association was found between hyperglycemia and hospital mortality, both in the bivariate and multivariate analysis, and in 2 articles this association was not demonstrated. For in-hospital mortality, the results of 11 articles included in this review were synthesized. The frequency of occurrence of heart failure was determined in 11 articles, finding a higher frequency in 9 of them. For in-hospital mortality, the results of 11 articles included in this review were synthesized and analyzed, in 8 the analysis was performed in non-diabetics, obtaining OR: 4.15, IC 95% (2.853-6.035), in 3 for diabetics obtaining OR 2.365 IC 95% (1.778- 3,146) and in 6 for the total population finding OR 3,314 (2,910-3,774). Conclusions: Hyperglycemia on admission is associated with increased mortality and frequency of occurrence of heart failure during hospitalization for myocardial infarction, with evidence of moderate quality.

The Role of Arterial Elasticity in Determining the Degree of Chronic Heart Failure in Myocardial Infarction.

Aim To study the left ventricular (LV) contractile and pumping function during the recovery phase following ligation of the anterior descending coronary artery (CA).Material and methods Cardiodynamic parameters were studied in Wistar rats 2-4 weeks after experimental myocardial infarction (MI). MI was induced by ligation of the anterior descending CA under zoletil anesthesia. LV catheterization was performed with a standard FTH-1912B-8018 PV catheter inserted into the LV through the right carotid artery.Results After the induction of MI, the mortality rate of animals was 50%. Survived animals developed significant LV dilatation and a decrease in ejection fraction (EF) by an average of 31%. However, major indexes of the pumping function, including minute volume, heart work, and maximum ejection velocity, were within a normal range whereas the maximum filling velocity was almost doubled. Approximately 50% of hearts with dilated LV had normal EF, delayed relaxation, and increased LV diastolic pressure, which qualified this group as a diastolic dysfunction group. The systolic dysfunction group with EF less than 50% of normal had similar values of myocardial contractility and relaxation but differed from the diastolic dysfunction group in more than 50% reduced maximum LV ejection velocity and 1.7 times increased elasticity of the arterial wall. A close inverse correlation was found between these values (r= -0.91).Conclusion The study results showed that, with a similar myocardial contractile function, the cardiac pumping function is determined by the elasticity of the aortic wall. Therefore, restriction of reactive fibrosis during MI is an important task of modern cardiology.

An image-driven micromechanical approach to characterize multiscale remodeling in infarcted myocardium

Myocardial infarction (MI) is accompanied by the formation of a fibrotic scar in the left ventricle (LV) and initiates significant alterations in the architecture and constituents of the LV free wall (LVFW). Previous studies have shown that LV adaptation is highly individual, indicating that the identification of remodeling mechanisms post-MI demands a fully subject-specific approach that can integrate a host of structural alterations at the fiber-level to changes in bulk biomechanical adaptation at the tissue-level. We present an image-driven micromechanical approach to characterize remodeling, assimilating new biaxial mechanical data, histological studies, and digital image correlation data within an in-silico framework to elucidate the fiber-level remodeling mechanisms that drive tissue-level adaptation for each subject. We found that a progressively diffused collagen fiber structure combined with similarly disorganized myofiber architecture in the healthy region leads to the loss of LVFW anisotropy post-MI, offering an important tissue-level hallmark for LV maladaptation. In contrast, our results suggest that reductions in collagen undulation are an adaptive mechanism competing against LVFW thinning. Additionally, we show that the inclusion of subject-specific geometry when modeling myocardial tissue is essential for accurate prediction of tissue kinematics. Our approach serves as an essential step toward identifying fiber-level remodeling indices that govern the transition of MI to systolic heart failure. These indices complement the traditional, organ-level measures of LV anatomy and function that often fall short of early prognostication of heart failure in MI. In addition, our approach offers an integrated methodology to advance the design of personalized interventions, such as hydrogel injection, to reinforce and suppress native adaptive and maladaptive mechanisms, respectively, to prevent the transition of MI to heart failure. Statement of significanceBiomechanical and architectural adaptation of the LVFW remains a central, yet overlooked, remodeling process post-MI. Our study indicates the biomechanical adaptation of the LVFW post-MI is highly individual and driven by altered fiber network architecture and collective changes in collagen fiber content, undulation, and stiffness. Our findings demonstrate the possibility of using cardiac strains to infer such fiber-level remodeling events through in-silico modeling, paving the way for in-vivo characterization of multiscale biomechanical indices in humans. Such indices will complement the traditional, organ-level measures of LV anatomy and function that often fall short of early prognostication of heart failure in MI.

MiR-96-5p regulates myocardial infarction-induced cardiac fibrosis via Smad7/Smad3 pathway.

Fibrotic remodelling contributes to heart failure in myocardial infarction. MicroRNAs (miRNAs) play a crucial role in myocardial fibrosis. However, current antifibrotic therapeutic strategies using miRNAs are far from effective. In this study, we aim to investigate the effect of miR-96-5p on cardiac fibrosis. Our work reveals a significant upregulation of miR-96-5p level in the ventricular tissues of myocardial infarction mice, as well as in neonatal rat cardiac fibroblasts stimulated with TGF-β or Ang II as shown by qPCR assay. In myocardial infarction mice, miR-96-5p knockdown using antagomir alleviates the aggravated cardiac fibrosis and exacerbated myocardial function caused by myocardial infarction surgery as shown by the echocardiography and Masson's staining analysis. In contrast, immunofluorescence staining results reveal that miR-96-5p overexpression in neonatal rat cardiac fibroblasts contributes to an increase in the expressions of fibrosis-associated genes and promotes the proliferation and differentiation of cardiac fibroblasts. Conversely, miR-96-5p downregulation using inhibitor presents adverse consequences. Furthermore, Smad7 expression is downregulated in fibrotic cardiac tissues, and the Smad7 gene is identified as a direct target of miR-96-5p by dual luciferase assay. Indeed, Smad7 knockdown weakens the anti-fibrotic effect of the miR-96-5p inhibitor on cardiac fibroblasts. Moreover, Smad3 phosphorylation is elevated in fibrotic cardiac tissues, and interestingly, the Smad3 inhibitor suppresses the profibrotic effect of the miR-96-5p mimic. Taken together, our findings demonstrate that the Smad7/Smad3 signaling pathway mediates the profibrotic effect of miR-96-5p in cardiac fibrosis.

Heart failure in myocardial infarction with non-obstructive coronary arteries: predictors and prognosis

Abstract Funding Acknowledgements Type of funding sources: None. Introduction Heart failure (HF) is a frequent complication of acute coronary syndromes (ACS). However, 5-15% of patients admitted with suspected acute myocardial infarction have no significant lesions on coronary angiography (>50%). Contrary to initial beliefs, MINOCA is not a benign disease, given that mortality and incidence of MACE is similar to ACS. Objective To evaluate predictors and prognosis of HF in the setting of MINOCA. Methods Based on a multicenter retrospective study, data collected from admissions between 2013 and 2020. Patients (pts) without data on cardiovascular history or uncompleted clinical data were excluded. Pts were divided in 2 groups (G): GA – pts without HF; GB - pts with HF during hospitalization. Results HF occurred in 63 (5.2%) out of 1218 pts with MINOCA. There were no differences between G regarding gender (p=0.779). GB pts were older (72±10 vs 65±13, p<0.001), had higher rates of arterial hypertension (88.9% vs 68.7%, p<0.001), diabetes (45% vs 27.5%, p=0.003), valvular disease (15.8% vs 2.1%, p<0.001), previous HF history (17.2% vs 6.2%, p=0.004), kidney dysfunction (15.1% vs 4.6%, p=0.006) and dementia (8.8% vs 0.7%, p<0.001). GA had higher rates of smoking habits (22.4% vs 3.3%, p<0.001). GB had higher heart rate at admission (92±25 vs 75±17, p<0.001), and higher rates of KK>1 (71.4% vs 6.3&, p<0.001), atrial fibrillation (25.5% vs 7.9%, p<0.001) and left branch bundle block (LBBB) (8.7% vs 1.4%, p=0.007). GB presented higher rates of kidney dysfunction (creatinine>2.0mg/dL) at admission (20.8% vs 4.8%, p<0.001)) and during hospital stay (31.6% vs 9.8%, p<0.001), lower haemoglobin levels at admission (13±1.8 vs 13.8±1.8, p=0.008) and during hospital stay (11.1±2.4 vs 12.7±1.8, p<0.001), higher BNP levels (BNP>400pg/ml) (100% vs 18.1%, p<0.001), and higher rates of left ventricle systolic dysfunction (LVEF<50%) (55.6% vs 17.6%, p<0.001). Logistic regression confirmed that KK>1 (p<0.001, OR 37.4, CI 13.6-102.7), LBBB (p=0.005, OR 10.1, CI 2.0-51.0), LV dysfunction (p=0.002, OR 8.3, CI 2.1-32.1) and smoking (p=0.046, OR 0.096, CI 0.01-0.96) were predictors of HF in the setting of MINOCA. Survival analysis confirmed GA had better prognosis regarding 1 year mortality compared to GB (p<0.001). Conclusion As expected, HF in the setting of MINOCA is associated with poorer prognosis. Several features may help predict the HF occurrence during hospitalizations, allowing an earlier treatment.

Comorbidity in acute heart failure complicating myocardial infarction

Aim. To study the relationship between comorbidity and acute heart failure (AHF) complicating myocardial infarction (MI). Material and methods . The analysis included 993 patients with MI from the registry of acute coronary syndrome RECORD-3. Killip class II-IV was recorded in every fifth patient (n=205). Hospital mortality was 6,3%. The mean age was 64,3 (63,5-65,0) years (men — 66,1%). All patients were divided into three groups depending on the number of comorbidities (type 2 diabetes, chronic kidney disease, atrial fibrillation, anemia, stroke, hypertension, obesity, peripheral atherosclerosis, thrombocytopenia). The first group included patients with no more than one disease (n=251), the second one — with 2 or 3 diseases (n=480), and the third one — with 4 or more diseases (n=262). Results. AHF detection rate increased in groups with increasing comorbidity: 12,3%, 17,9% and 33,6%, respectively (p<0,0001). Regardless of the initial therapy, in patients of the first group without AHF the hospital mortality rate did not exceed 1%. In patients of the third group with Killip class II-IV AHF the hospital mortality was the highest and also did not depend on the choice of treatment strategy (24,6% with conservative management, 31,6% with percutaneous coronary intervention (PCI)). PCI made it possible to reliably (p<0,05) reduce the risk of hospital mortality in patients of the second and third groups without AHF relative risk 4,3 (1,0-19,9) and 4,2 (1,1-18,3), respectively. Analysis of a 1-year follow-up revealed that AHF is a death predictor after hospital discharge independent of the comorbidity severity: 11,1%, 13,3%, and 14,3%, respectively. In patients without AHF a 1-year mortality increased from the first to the third group: 1,1%, 5,8% and 7,0%, respectively (p=0,043). Conclusion . Сomorbidity is an independent predictor of heart failure in MI, and their combination is associated with the most unfavorable in-hospital prognosis, regardless of the treatment strategy. The greatest advantage of PCI for reducing the hospital mortality rate was obtained in patients with comorbidity and without manifestations of AHF.

β-Adrenergic Blocker, Carvedilol, Abolishes Ameliorating Actions of Adipose-Derived Stem Cell Sheets on Cardiac Dysfunction and Remodeling After Myocardial Infarction.

Treatment of myocardial infarction (MI) includes inhibition of the sympathetic nervous system (SNS). Cell-based therapy using adipose-derived stem cells (ASCs) has emerged as a novel therapeutic approach to treat heart failure in MI. The purpose of this study was to determine whether a combination of ASC transplantation and SNS inhibition synergistically improves cardiac functions after MI.Methods and Results:ASCs were isolated from fat tissues of Lewis rats. In in vitro studies using cultured ASC cells, mRNA levels of angiogenic factors under normoxia or hypoxia, and the effects of norepinephrine and a β-blocker, carvedilol, on the mRNA levels were determined. Hypoxia increased vascular endothelial growth factor (VEGF) mRNA in ASCs. Norepinephrine further increased VEGF mRNA; this effect was unaffected by carvedilol. VEGF promoted VEGF receptor phosphorylation and tube formation of human umbilical vein endothelial cells, which were inhibited by carvedilol. In in vivo studies using a rat MI model, transplanted ASC sheets improved contractile functions of MI hearts; they also facilitated neovascularization and suppressed fibrosis after MI. These beneficial effects of ASC sheets were abolished by carvedilol. The effects of ASC sheets and carvedilol on MI heart functions were confirmed by Langendorff perfusion experiments using isolated hearts. ASC sheets prevented cardiac dysfunctions and remodeling after MI in a rat model via VEGF secretion. Inhibition of VEGF effects by carvedilol abolished their beneficial effects.

The Effect of Short-Term Exposure in PM0.1 on Cardiac Remodeling and Dysfunction in Myocardial Infraction Mice

We aimed to illustrate the association between short-term exposure PM0.1 and heart failure in myocardial infarction (MI) mice. Six-week-old ICR mice were divided into three groups randomly: sham group, MI group and MI exposure group, 12 mice in each group. LAD ligation operation was performed in MI group and MI exposure group. After postoperative two weeks MI exposure mice were put into ventilation chamber which filled with 500ug/m3 PM0.1 for 6 hours per day, while MI group mice and sham group mice were cultivated in normal environment. After exposure 8 weeks, we use Vevo 2100 machine to acquire heart function measurements. Then we collected blood sample and killed mice to obtain heart samples. The proliferation of myocardium were measured by immunofluorescence. Elisa was performed to detect the catecholamine expression in plasma. The changes of collagen were measured by Sirus red stain method. Compared with the sham group, the EF and FS in the MI group were significantly decreased (p<0.05), and MI exposure group showed higher amplitude decrease. The immunofluorescence result showed that the number of proliferating cell in MI exposure group did not change significantly. In addition, the IL-11 in the peripheral blood of MI exposure group did not change significantly, while Sirus red stain showed the content of collagen in MI exposure group increased significantly (p<0.05). In conclusion, short-term exposure in PM0.1 can exacerbate cardiac remodeling and dysfunction, while it had effect neither on IL-11 in peripheral blood nor on myocyte proliferation.

Epidemiology of heart failure in myocardial infarction treated with primary angioplasty: Analysis of the Codi IAM registry

Introduction and objectivesThe epidemiology of heart failure (HF) that complicates ST-segment elevation myocardial infarction (STEMI) is not well defined. Our aim was to analyze the epidemiology and prognosis of HF that complicates STEMI treated with primary percutaneous coronary intervention (PCI). MethodsMulticentre registry of 14070 patients with STEMI treated with primary PCI from January 2010 to December 2015. ResultsPatients with HF were older, more frequently female, and diabetic and had chronic ischaemic heart disease. Only 10.3% of patients with STEMI treated with primary PCI had HF on admission and the majority of them had the mildest form (Killip–Kimball II 77.8%). HF was associated with high mortality (30-day mortality was 2.9% of patients in Killip–Kimball I, 9.5% of Killip–Kimball II and 17.4% in Killip–Kimball III, P<.005, and 1-year mortality in patients who survived 30 days was 2.9%, 9.3% and 14.3%, P<.005, respectively). Both the presence of Killip–Kimball class II and III were independently associated with 30-day and 1-year mortality in 30-day survivors. Up to 6% and 15% of patients in Killip–Kimball II and III on admission worsened to cardiogenic shock, and the onset of cardiogenic shock during hospitalization was independently associated with mortality at 30-day and 1-year follow-up. ConclusionsHF complicates 10.3% of patients with STEMI treated with primary PCI and it was associated with a higher risk of developing cardiogenic shock and with 30-day and 1-year mortality in 30-day survivors. In this high-risk population, primary PCI and posterior medical treatment should be prioritized to avoid worsening of HF.

O19-2 - Risk of Heart Failure in Myocardial Infarction with Reduced, mid Range and Preserved Ejection Fraction

O19-2 - Risk of Heart Failure in Myocardial Infarction with Reduced, mid Range and Preserved Ejection Fraction

FORMULATION AND EVALUATION OF MICROSPHERES FOR NASAL DELIVERY OF ANTI-HYPERTENSIVE DRUG

Lisinopril is used in the treatment of hypertension and heart failure in myocardial infarction and also in diabetic nephropathy. It is very poorly absorbed from GIT. Intranasal administration is an ideal alternative to the parenteral route for systemic drug delivery. Formulating multiparticulate system with mucoadhesive polymers may provide a significant increase in the nasal residence time. The microspheres prepared by emulsion solvent evaporation method were characterized for encapsulation efficiency, drug loading, particle size, surface morphology, degree of swelling, ex vivo mucoadhesion, drug release and ex vivo diffusion studies. Entrapment efficiency of microspheres was in range of 84.95±0.50% to 97.44±0.61% mucoadhesion was 83.76% and 94.41% and drug release up to 40 minutes was 53.66% to 88.32%. In ex vivo studies, the microspheres showed good bioavailability by nasal route compared to oral drug administration. Both in vitro and in vivo studies conclude that combination of Carbopol and HPMC based microspheres are better than single carbopol-based formulation for the delivery of lisinopril.

0289 : Correlation of higher serum uric acid and severity of congestive heart failure in myocardial infarction: prospective study

Serum uric acid (SUA) reflects xanthine oxidase activity's level and oxidative stress’ production. Hyperuricemia has been identified as a marker of poor prognosis in patients with congestive heart failure (CHF) after acute myocardial infarction (AMI). To assess SUA levels determined on admission as a potential predictor of severity of the CHF in AMI patients. Data for this prospective observational study were collected from the ACS database register created on January 2015. We included consecutive patients with verified AMI admitted within 48 hours since the symptom onset during the period between January and November 2015. Clinical, biological and echocardiographic data were collected through direct contacts with patients during their hospitalization. The study was conducted on two groups: Fifty four patients (42.1%) with high level of SUA on admission were allocated to the group I and were compared to patients of group II (n=74, 57.9%) with normal SUA. Group I patients had less previous history of hypertension, dyslipidemia and smoking (37.8% vs 45.3%; 10.8% vs 17.6% and 51.3% vs 58.8% respectively) but more history of stroke 5.4% vs 1.96%. On admission, mean HR was higher in group 1 than in group 2 (83,73 +/– 17,19 vs 78,37+/–14,64 bpm). Mean SBP was lower in group 1 than in group 2. The mean LVEF was significantly lower in group 1 (40%+/–9,675 vs 45,67%+/–7,528 ; p= 0.03). This observational cohort identified a close relationship between SUA and Killip classification. Patients who developed short-term CHF had higher concentrations of SUA; the severity of the congestion was proportional to the value of SUA (Killip III-IV: 27.02% vs 7.8%; p =0.04). Our results suggest that hyperuricemia after myocardial infarction is associated with the severity of CHF. The serum level of uric acid is a suitable marker to predict adverse events related to myocardial infarction. The author hereby declares no conflict of interest

Renal failure in myocardial infarction with cardiogenic shock - comparison of established and novel biomarkers - a biomarker substudy of the IABP-SHOCK II-trial

Background: Impairment of renal function is an important prognostic factor in acute coronary syndromes. In cardiogenic shock loss of renal function is one important sign of inadequate end-organ perfusion. The role of the novel biomarkers Neutrophil Gelatinase-Associated Lipocalin (NGAL), Kidney Injury Molecule 1 (KIM1) and Cystatin C for renal injury in comparison to established serum creatinine has never been investigated before. Methods: In the randomized Intraaortic Balloon Pump in Cardiogenic Shock II (IABP-SHOCK II)-trial 600 patients with Cardiogenic Shock (CS) complicating acute myocardial infarction undergoing early revascularization were assigned to therapy with IABP or no IABP. In 190 patients blood samples were collected directly during primary primary coronary intervention, on day one, and day two after randomization. Blood was centrifuged immediately after sample drawing and serum frozen at -87° C. NGAL, KIM1 and Cystatin C were measured with standard ELISA-Kits, Creatinine was assessed with routine laboratory measurement. All-cause mortality at 30 days was used for outcome assessment. Results: Survivors had lower levels of creatinine (109 [IQR 90; 141] vs. 138 [IQR 102; 186] μmol/L; p<0.001) and NGAL (915 [IQR 568; 1415] vs. 1091 [IQR 769; 2229] ng/mL; p=0.01) than non-survivors at baseline, whereas there was no significant difference for KIM1 (134 [IQR 119; 164] vs. 123 [IQR 108; 178] pg/mL; p=0.82) and Cystatin C (3084 [IQR 2510; 3596] vs. 3366 [IQR 2626; 3778] ng/mL; p=0.16). In repeated measures analysis of variance over all three measurements creatinine (p=0.04) and NGAL (p=0.04) showed significant differences in contrast to KIM1 (p=0.21) and Cystatin C (p=0.42). Receiver operator characteristics (ROC) showed highest values for the area under the curve (AUC) in prediction of 30 day mortality for creatinine at all three time points (AUC baseline 0.65; day one 0.75; day two 0.78), NGAL showed the second best performance (AUC baseline 0.62; day one 0.60; day two 0.66). In c-statistics creatinine showed significant higher AUC over NGAL on day one and day two (p=0.003; p=0.03; respectively) and significant higher AUC at all time points in comparison to KIM1 and Cystatin C. Conclusion: Renal failure has significant impact on outcome in cardiogenic shock. Of novel markers of renal injury NGAL showed the best performance in prediction of 30 day mortality, but was inferior to established serum creatinine measurements.

THERAPEUTIC RELEVANCE OF ALTERED CYTOKINE EXPRESSION

Cytokines and their receptors have numerous physiological functions. Altered concentrations of these mediators are associated with various afflictions. For example, over-expression of cytokines has been associated with altered drug concentrations and activity. Greater concentrations of cardiovascular drugs have been observed in humans and laboratory animals with various types of inflammatory disorders compared to healthy controls. Interestingly, the observed higher concentrations of drugs such as propranolol and verapamil have not been associated with increased effects. Indeed, reduced response to these cardiovascular drugs is observed, suggestive of cytokine-mediated downregulation of receptors. Increased cytokine concentrations have also been associated with decreased response to drugs used in treatment of other disorders such as AIDS, asthma and psychiatric diseases. This reduced response to drug in the presence of altered cytokine concentrations is especially relevant to the elderly population which has a greater incidence of multiple diseases and elevated concentrations of various cytokines compared to younger individuals. Furthermore, inflammatory conditions and their accompanied increased over-expression of cytokines are suggested to be the main determinants of therapeutic failure in myocardial infarction and angina. Therefore, altered cytokine concentrations may influence therapeutic outcomes of pharmacotherapy and result in treatment failure.

Acute heart failure in myocardial infarction

Congestive heart failure after acute myocardial infarction can extend the area of infarction by worsening the oxygen supply-demand balance. Appropriate treatment requires insight into this pathophysiologic condition and knowledge of the effects of the various therapies available. Understanding of the role of vasodilating and inotropic agents and of mechanical interventions such as ventilation with PEEP is an important aspect of treatment.

The management of acute coronary insufficiency

1. Coronary insufficiency is a pathophysiologic state that can initiate lethal cardiac arrhythmias in the absence of myocardial necrosis. Patients with suspected coronary insufficiency should be monitored until they are stabilized and a diagnosis is confirmed. 2. Early and adequate intravenous antiarrhythmic prophylaxis with lidocaine to raise the fibrillation threshold in the setting of coronary insufficiency can prevent primary ventricular fibrillation. Classic "warning arrhythmias" are not predictive of ventricular fibrillation. Their persistence during adequate antifibrillatory prophylaxis does not indicate therapeutic failure. 3. The isoenzyme of creatine phosphokinase, CPK-MB, is an extremely sensitive and specific indicator of myocardial necrosis if measured serially during the 24 hours following the onset of symptoms suggesting coronary insufficiency. It may prove most useful in eliminating the false positive diagnosis of myocardial infarction in difficult clinical cases. 4. The management of heart failure in myocardial infarction requires an understanding of the relationship between ventricular preload and the cardiac output. The treatment of clinical manifestations of an elevated ventricular preload in asymptomatic patients is not justified and may be detrimental. In symptomatic patients, however, judicious manipulation of ventricular preload should be the first therapeutic consideration, and an optimal filling pressure should be achieved and maintained when other determinants of the cardiac output are manipulated. 5. Indications for the prophylactic insertion of a temporary transvenous pacing electrode for heart block associated with myocardial infarction must be individualized. Most authorities agree that prophylactic pacing may be justified in patients with evidence of new infranodal block involving two of the three fascicles. Patients with bifascicular block who progress to complete heart block transiently may benefit from permanent transvenous pacemaker insertion before discharge. 6. Hospitalized patients with persistent pain of suspected cardiac origin but without evidence of myocardial infarction can be studied safely with coronary angiography. A small percentage will be normal or have diffuse disease that is inoperable. Of those with operable disease, short-term mortality appears to be similar for medical and surgical therapy. 7. Patients with an uncomplicated myocardial infarction may be safely discharged from thehospital by day 7-10. 8. Experimental evidence indicates that modification of infarct size is possible. Application of these concepts to human subjects presently is limited by the absence of a proved method of measuring infarct size in vivo in humans.

Pump failure in myocardial infarction.

To find a clue to the treatment, pathophysiology of myocardial infarction with pump failure was studied. Pump failure was divided into two subsets, pump failure immediately after the initial attack and pump failure over two weeks after the initial attack. In each subset, characteristics of pump failure in myocardial infarction were discussed.

Respiratory failure in myocardial infarction

Respiratory failure in myocardial infarction

Chest x-ray film in acute myocardial infarction.

A total of 185 chest x-ray films taken on 50 consecutive admissions to a coronary care unit were assessed independently for specific abnormalities by three observers. The commonest abnormality was upper lobe pulmonary venous congestion. When this was present by itself it did not appear to affect prognosis. Pulmonary oedema occurred in 12 of the patients, was associated with more pronounced pulmonary venous congestion (but not necessarily with cardiac enlargement), and usually cleared within five days. Generalized cardiac enlargement and septal lines were rarely seen. Clinically silent non-segmental shadows were found in six patients.No consistent change in radiological abnormality was found in the first three days after infarction, but thereafter a gradual improvement occurred, so that before discharge the x-ray picture was nearly normal. There was good correlation between the presence and extent of lung crepitations and the presence of pulmonary oedema on the chest x-ray film.It is suggested that the chest x-ray film is a useful additional index of the severity of heart failure in myocardial infarction.

The treatment of heart failure and the use of digitalis in myocardial infarction

1. (1) To deal accurately with the therapy of heart failure, we must thoroughly understand the condition and the drugs at our command. 2. (2) Treatment of acute left heart failure in myocardial infarction consists primarily of oxygen with anti-foaming therapy, morphine, tourniquets, and digitalis. 3. (3) Treatment of chronic congestive failure in myocardial infarction consists primarily of rest, low-sodium intake, digitalis, oxygen, and mercurial diuretics. 4. (4) The indications for and the actions of digitalis in heart failure following myocardial infarction are discussed. 5. (5) Digitalis should not be given parenterally in myocardial infarction unless acute pulmonary edema exists or there is no other feasible portal of entry. Lanatoside D or Lanoxin is preferred for this and Lanoxin, digitoxin or gitalin is preferred for oral use. 6. (6) The precautions in the use of digitalis, the signs of toxicity, and the therapy of digitalis toxicity are discussed.