Prognosis Of Ischemic Heart Disease Research Articles

Usefulness of cardiac MRI in the prognosis and follow-up of ischemic heart disease

Cardiac magnetic resonance imaging (MRI) is an important tool that makes it possible to evaluate patients with cardiovascular disease; in addition to infarction and alterations in myocardial perfusion, cardiac MRI is useful for evaluating other phenomena such as microvascular obstruction and ischemia. The main prognostic factors in cardiac MRI are ventricular dysfunction, necrosis in late-enhancement sequences, and ischemia in stress sequences. In acute myocardial infarction, cardiac MRI can evaluate the peri-infarct zone and quantify the size of the infarct. Furthermore, cardiac MRI's ability to detect and evaluate microvascular obstruction makes it a fundamental tool for establishing the prognosis of ischemic heart disease. In patients with chronic ischemic heart disease, cardiac MRI can detect ischemia induced by pharmacological stress and can diagnose infarcts that can be missed on other techniques.

Utilidad de la RM cardíaca en el pronóstico y seguimiento de la cardiopatía isquémica

Cardiac magnetic resonance imaging (MRI) is an important tool that makes it possible to evaluate patients with cardiovascular disease; in addition to infarction and alterations in myocardial perfusion, cardiac MRI is useful for evaluating other phenomena such as microvascular obstruction and ischemia. The main prognostic factors in cardiac MRI are ventricular dysfunction, necrosis in late enhancement sequences, and ischemia in stress sequences. In acute myocardial infarction, cardiac MRI can evaluate the peri-infarct zone and quantify the size of the infarct. Furthermore, cardiac MRI's ability to detect and evaluate microvascular obstruction makes it a fundamental tool for establishing the prognosis of ischemic heart disease. In patients with chronic ischemic heart disease, cardiac MRI can detect ischemia induced by pharmacological stress and can diagnose infarcts that can be missed on other techniques.

A comparative analysis of leukocyte and leukocyte subtype counts among isolated systolic hypertensive, systo-diastolic hypertensive, and non-hypertensive patients

Isolated systolic hypertension (ISHT) is a subtype of hypertension (HT) that often exhibits wide pulse pressure, and pulse pressure has a strong predictive value for future adverse cardiovascular events. Previous studies have shown the effects of leukocyte count on the prognosis of ischaemic heart disease and HT. Thus, in this cross-sectional study, we analysed the relationship between leukocyte counts and subtypes in HT and non-HT groups. The study population consisted of 960 consecutive patients who were admitted to the outpatient clinic of our hospital. After ambulatory blood pressure values were assessed, the participants were divided into three groups: ISHT (n = 98), systo-diastolic hypertensives (SDHT, n = 405), and non-hypertensives (non-HT, n = 457). The subjects in the ISHT group were older than those in the SDHT and non-HT groups (64 ± 10, 53 ± 12, and 52 ± 13, respectively; p < 0.001). The leukocyte and neutrophil counts and neutrophil/lymphocyte (NL) ratios were significantly different in all groups. In subgroup analysis, the leukocyte count, neutrophil count, and N/L ratio were higher in the ISHT and SDHT groups than in the non-HT group (p < 0.001 for all). The leukocyte count, neutrophil count, and N/L ratio were significantly higher in the ISHT group than in the SDHT group (p = 0.023, p = 0.007, p = 0.010, respectively). Neutrophil count (p = 0.012; OR = 1.229, 95% CI 1.046-1.444) was an independent risk factor for ISHT in multivariate logistic regression analysis. The leukocyte and neutrophil counts and N/L ratios were higher in the ISHT group than in the SDHT and non-HT groups. High neutrophil count was an independent predictor of ISHT.

Increased QT interval dispersion in diagnosis of acute coronary syndrome with atypical symptoms and EKG.

INTRODUCTION EKG remains a highly valuable tool for heart disease management. Corrected QT interval dispersion is a useful EKG parameter to assess prognosis in ischemic heart disease and specifically acute coronary syndrome. Understanding QT interval physiopathology helps assess importance of QT measurement in this context. Although increased QT dispersion is an ominous prognostic marker, its utility has not been evaluated for all types of acute coronary syndrome, even though in many circumstances it is the only tool available for diagnosing patients with equivocal EKG signs and/or atypical symptoms. OBJECTIVE Describe corrected QT interval dispersion in acute coronary syndrome in three groups of patients-with ST elevation, without ST elevation, and without ST elevation with equivocal EKG signs-admitted to the intensive care unit of Celestino Hernández Robau University Hospital in Santa Clara, Cuba, from January 2010 through June 2011. METHODS A descriptive retrospective study was conducted in 194 patients admitted with diagnosis of acute coronary syndrome. QT interval was measured and its dispersion calculated for the first EKG after symptom onset. Patterns were assessed for typical and atypical clinical presentations, and unequivocal and equivocal EKG signs. RESULTS Nonclassifiable acute coronary syndrome was found in 6.7% of patients (13/194), the majority of whom had increased QT dispersion (76.9%, 10/13). There were significant differences in QT dispersion patterns between patients with typical and atypical presentations and between patients with equivocal and unequivocal EKG findings. In non-ST elevation acute coronary syndrome and nonclassifiable acute coronary syndrome with increased dispersion, atypical presentation was the most common (65.5%, 19/29; and 90%, 9/10, respectively). CONCLUSION Corrected QT interval dispersion is a useful diagnostic tool for acute coronary syndrome, especially when patients present with atypical symptoms and equivocal EKG findings. Thus, it is a low-cost alternative in management of acute coronary syndrome in resource-poor settings.

Assessment of left ventricular ejection fraction using the wall motion score index in cardiac magnetic resonance imaging

Left ventricular ejection fraction (LVEF) is an important indicator of left ventricular function and of the severity and prognosis of ischaemic heart disease. Assessment of regional function using the wall motion score index (WMSI) is an alternative means of evaluating left ventricular function. We attempted to evaluate LVEF by a method using the WMSI with cardiac magnetic resonance imaging (MRI). One hundred and twenty-two patients referred for evaluation of heart disease had rest WMSI evaluation by cardiac MRI. The WMSI was evaluated using the 16-segment model and score proposed by the American Society of Echocardiography. In our first group of 80 patients, a correlation between WMSI and cardiac MRI LVEF was established and a regression equation was derived. This regression equation was then used in 42 consecutive patients to compare WMSI LVEF with the gold standard MRI LVEF. In the first 80 patients, MRI LVEF and WMSI correlated very well (r=0.93). Similarly, in the second group of 42 patients, WMSI LVEF derived from the regression equation correlated very well with MRI LVEF (r=0.94). An objective evaluation of LVEF can be easily made using the WMSI with cardiac MRI, which correlates very well with standard MRI planimetric methods.

Effects of Intravenous Nicorandil on the Mid-Term Prognosis of Patients With Acute Heart Failure Syndrome

Acute heart failure syndrome (AHFS) remains a major clinical challenge because of its poor prognosis. Nicorandil, a hybrid compound of a potassium-channel opener and nitric oxide donor, has been reported to improve the prognosis of ischemic heart disease. We sought to evaluate the effect of intravenous nicorandil on the mid-term prognosis of AHFS. A total of 402 consecutive patients who were hospitalized for AHFS were divided into 2 groups according to the use of intravenous nicorandil: 78 patients in the Nicorandil group and 324 patients in the Control group. During the 180-day follow-up, death or rehospitalization for heart failure occurred in 7 patients in the Nicorandil group (9.0%) and in 75 patients (23.2%) in the Control group. Event-free survival rates were significantly higher in the Nicorandil group than in the Control group (P=0.006). Multivariate Cox hazard analysis revealed that age (hazard ratio (HR)=1.066, P<0.0001), systolic blood pressure (HR=0.983, P=0.0023), New York Heart Association class III/IV (HR=6.550, P<0.0001), log creatinine (HR=3.866, P=0.0106), and use of intravenous nicorandil (HR=0.179, P<0.0001) were significant predictive factors for the occurrence of death or rehospitalization for heart failure. Intravenous nicorandil treatment from the urgent phase of AHFS may improve the prognosis.

Ischaemic heart disease in women: are there sex differences in pathophysiology and risk factors?: Position Paper from the Working Group on Coronary Pathophysiology and Microcirculation of the European Society of Cardiology

Cardiovascular disease (CVD) is the leading cause of death in women, and knowledge of the clinical consequences of atherosclerosis and CVD in women has grown tremendously over the past 20 years. Research efforts have increased and many reports on various aspects of ischaemic heart disease (IHD) in women have been published highlighting sex differences in pathophysiology, presentation, and treatment of IHD. Data, however, remain limited. A description of the state of the science, with recognition of the shortcomings of current data, is necessary to guide future research and move the field forward. In this report, we identify gaps in existing literature and make recommendations for future research. Women largely share similar cardiovascular risk factors for IHD with men; however, women with suspected or confirmed IHD have less coronary atherosclerosis than men, even though they are older and have more cardiovascular risk factors than men. Coronary endothelial dysfunction and microvascular disease have been proposed as important determinants in the aetiology and prognosis of IHD in women, but research is limited on whether sex differences in these mechanisms truly exist. Differences in the epidemiology of IHD between women and men remain largely unexplained, as we are still unable to explain why women are protected towards IHD until older age compared with men. Eventually, a better understanding of these processes and mechanisms may improve the prevention and the clinical management of IHD in women.

Effects of Nicorandil on Cardiovascular Events in Patients With Coronary Artery Disease in The Japanese Coronary Artery Disease (JCAD) Study

Nicorandil has cardioprotective effects in the ischemic myocardium, mimicking ischemic preconditioning, and is thus expected to improve the prognosis of ischemic heart disease (IHD). As part of the Japanese Coronary Artery Disease (JCAD) Study, a multicenter collaborative prospective observational study of a large cohort of coronary artery disease patients, the effect of nicorandil on outcome was examined. In total, 2,558 patients with nicorandil treatment and controls subjected to propensity score matching were eligible among 13,812 patients registered in the JCAD study. The mean follow-up interval was 2.7 years. The primary endpoint, death from all causes, was significantly lower, by 35% (hazard ratio 0.65, P=0.0008), in the nicorandil group than in the control group. There were also significant reductions in secondary endpoints, including cardiac death (56%), fatal myocardial infarction (56%), cerebral or vascular death (71%), and congestive heart failure (33%) in the nicorandil group, with no excess of deaths from other non-cardiovascular causes. Treatment with nicorandil reduced the number of deaths from all causes to a similar extent with or without treatment with sulfonylureas. The reduction in cardiovascular death with nicorandil was large in patients with IHD, which has important implications for treatment.

Differenzierung von malignen und nichtmalignen, inflammatorischen Perikardergüssen mit Biomarkern

Disorders of the pericardium are commonly associated with pericardial effusion. Its etiology comprises a broad spectrum of diseases including also malignancies. Pericardiocentesis, pericardioscopy and targeted epicardial biopsy with consecutive pericardial fluid and epicardial biopsy analysis by cytology, molecular biology and immunology establish the underlying etiology in the majority of cases. Of particular therapeutic and prognostic importance is the definite differentiation of malignant pericardial effusion from benign pericardial effusion. Biomarkers for cardiovascular diseases can be divided into biochemical, histological, immunologic, serologic and molecular markers as well as imaging biomarkers. Biomarkers have proven to be useful in the diagnosis, differential diagnosis and prognosis of ischemic heart disease and heart failure. With respect to pericardial disorders, a comprehensive approach combining clinical information, imaging biomarkers, biomarkers of pericardial effusion and analysis of epicardial biopsies often leads to the definite etiologic diagnosis of pericardial effusion. Computed tomography and magnetic resonance imaging allow further characterization of the effusion and, of note, also of the surrounding tissue, which is of particular interest in case of malignancies. Biomarkers of pericardial effusion include biochemical markers, autoantibodies, tumor markers, and cytokines. Analysis of pericardial fluid specific gravity, protein level and lactate dehydrogenase (LDH) separates transudates from exsudates. High adenosine deaminase levels (ADA) and low levels of carcinoembryonic antigen (CEA) in the pericardial effusion are observed in tuberculous pericarditis allowing the differentiation from malignant pericardial effusion. Additional markers, such as interferon and lysozyme, have also been suggested for the diagnosis of tuberculous pericarditis. Tumor markers in pericardial fluid have been used to diagnose malignant pericarditis. CEA levels are significantly higher in malignant than benign effusion. By a cutoff level of CEA > 5 ng/ml the diagnostic sensitivity and specificity are 75% and 100%, respectively, in the diagnosis of malignant pericardial effusion. Further analysis of cytokines and mediators, serologic, immunologic and inflammatory markers may help to understand the pathophysiology of the pericardial disease and provide useful diagnostic information.

Relation between elevated high‐sensitivity C‐reactive protein and anti‐mitochondria antibody in patients with systemic sclerosis

Systemic sclerosis (SSc) is a systemic connective tissue disease of unknown etiology which presents immunological, vascular and connective tissue abnormalities. C-reactive protein (CRP) has been used for the evaluation of inflammation in patients with infection and inflammatory diseases. Recently, high-sensitivity CRP has been shown to reflect mild and/or moderate inflammation for the prognosis of ischemic heart disease. High-sensitivity CRP was measured for the evaluation of mild and/or moderate inflammation in SSc. Forty SSc patients (male : female, 7:33; age, 16-78 years; mean, 61.9 years) were studied. High-sensitivity CRP was measured with a nephelometric assay. The detection limit was 0.0036 mg/dL, linearity from 0.015-1.5 mg/dL. The distribution of high-sensitivity CRP showed 26 cases (65.0%) low, three cases (7.5%) mild, four cases (10.0%) moderate, four cases (10.0%) high and three cases (7.5%) highest. The occurrence rate of anti-mitochondria antibody in high-sensitivity CRP elevated SSc patients (8/14, 57.1%) was significantly elevated compared with that of high-sensitivity CRP low SSc patients (3/26, 11.5%) (P < 0.01). These results led us to the conclusion that elevated high-sensitivity CRP shows relation to the occurrence of anti-mitochondria antibody.

Impact of chronic gliclazide therapy in the nuclear oxidative stress and insulin-resistance levels in an animal model of diabetes

Introduction: Type 2 diabetes (DM) is associated with a higher incidence and worse prognosis of ischemic heart disease. High levels of insulin-resistance and nuclear oxidative stress, common in DM, may be involved. However, the mechanisms of these changes in DM and their modulation by chronic administration of gliclazide (a sulphonylurea) are not yet fully known.

Mo-P4:237 Clinical course and prognosis of ischemic heart disease with stable angina pectoris (DATA of A5-year study)

Mo-P4:237 Clinical course and prognosis of ischemic heart disease with stable angina pectoris (DATA of A5-year study)

Chordal cutting: a new therapeutic approach for ischemic mitral regurgitation.

Mitral regurgitation (MR) conveys adverse prognosis in ischemic heart disease. Because such MR is related to increased leaflet tethering by displaced attachments to the papillary muscles (PMs), it is incompletely treated by annular reduction. We therefore addressed the hypothesis that such MR can be reduced by cutting a limited number of critically positioned chordae to the leaflet base that most restrict closure but are not required to prevent prolapse. This was tested in 8 mitral valves: a porcine in vitro pilot with PM displacement and 7 sheep with acute inferobasal infarcts studied in vivo with three-dimensional (3D) echo to quantify MR in relation to 3D valve geometry. In all 8 valves, PM displacement restricted leaflet closure, with anterior leaflet angulation at the basal chord insertion, and mild-to-moderate MR. Cutting the 2 central basal chordae reversed this without prolapse. In vivo, MR increased from 0.8+/-0.2 to 7.1+/-0.5 mL/beat after infarction and then decreased to 0.9+/-0.1 mL/beat with chordal cutting (P<0.0001); this paralleled changes in the 3D leaflet area required to cover the orifice as dictated by chordal tethering (r(2)=0.76). Cutting a minimum number of basal chordae can improve coaptation and reduce ischemic MR. Such an approach also suggests the potential for future minimally invasive implementation.

Molecular mechanisms of apoptosis in the cardiac myocyte.

Cardiac myocytes can undergo programmed cell death in response to a variety of insults and apoptotic elimination of myocytes from the adult myocardium can lead directly to cardiomyopathy and death. Although it remains to be shown that therapy specifically targeting apoptosis will improve the prognosis of ischemic heart disease or heart failure, a number of studies in the past year have shed light on potential ways to intervene in the process. Progress in the past year includes a better understanding of the importance of mitochondria-initiated events in cardiac myocyte apoptosis, of factors inducing apoptosis during hypoxia, and of the dual pro-apoptotic and anti-apoptotic effects of hypertrophic stimuli such as beta-adrenoceptor agonists, nitric oxide and calcineurin. Further evidence supports the pathophysiologic relevance of apoptosis in human heart disease. The tracking of cytoprotective and apoptotic signal transduction pathways has revealed important new insights into the roles of the mitogen-activated protein (MAP) kinases p38, extracellular signal regulated kinase (ERK) and c-Jun N-terminus kinase (JNK) in cardiac cell fate.

Performing the exercise test

Exercise testing is useful in assessing physical fitness, determining functional capacity, diagnosing ischemic heart disease, defining the prognosis of ischemic heart disease, developing an exercise prescription, and guiding cardiac rehabilitation. This article outlines the current indications, contraindications, and special considerations for exercise testing. Specific protocols are discussed along with physician responsibilities for performing this procedure. A summary of current testing equipment is included.

4.13 Value of gated SPECT ejection fraction and ventricular volumes in diagnosis and prognosis of ischaemic heart disease

4.13 Value of gated SPECT ejection fraction and ventricular volumes in diagnosis and prognosis of ischaemic heart disease

Clinical Characteristics and EPS-guided Therapy in 142 Cases of Sustained Ventricular Tachycardia.

One hundred and forty-two consecutive patients with sustained monomorphic ventricular tachycardia (VT) were investigated. Only 26.1% of VTs were associated with ischemic heart disease (IHD). The induction rate of sustained VT upon electrophysiologic study (EPS) was 82.9% in patients with IHD and 65.3% in non-IHD. Of 76 inducible sustained VTs, pharmacologic therapy was finally selected in 35 cases, ablative therapy in 25 and surgical therapy in 12. Long-term prognosis was compared between groups divided according to type of ventricular arrhythmia induced at final EPS after antiarrhythmic therapy as follows: Group A: complete suppression of VT, Group B: clinical or non-clinical nonsustained VT, Group C: clinical sustained VT. The event rate in IHD was 6.3% in Group A, 44.4% in Group B and 100% in Group C. In non-IHD, the event rate was 24.0%, 25.0% and 75.0% (Groups A, B and C, respectively). Complete suppression of VT showed a good prognosis in IHD, however, a slightly higher recurrence rate was observed in non-IHD. In ablative therapy, some recurrences and sudden deaths were observed in spite of complete suppression of both VTs in both the IHD and non-IHD groups. Review of the efficacy of antiarrhythmic procedures is recommended during the follow-up period.

Clinical vs Nuclear Laboratory Diagnosis of Congestive Heart Failure

I enjoyed reading the excellent article by Marantz and associates 1 on whether clinical evaluation is as useful as radionuclide ventriculography in the management of patients with congestive heart failure. I agree completely with their conclusion that the clinical diagnosis of congestive heart failure, based on clinical evaluation and chest roentgenogram, is a valid predictor of mortality and provides information independent of the radionuclide left ventricular ejection fraction in determining prognosis in these patients. In this era of high technology, laboratory studies cannot substitute for a careful clinical assessment. The authors are so correct when they said Rather, it is the thorough clinician who judiciously orders and interprets tests of cardiac function who can best make an accurate prognosis. 1 I would like to make three comments. First, although the title of the article is Prognosis in Ischemic Heart Disease, the text concerns exclusively congestive heart failure, one of the

Generation and localisation of monoclonal antibodies against fibroblast growth factors in ischaemic collateralised porcine myocardium.

The collateral circulation plays a critical role in the prognosis of ischaemic heart disease, with a clear correlation between neovascularisation, infarction, and tissue recovery. The aim of the study was to address the question of whether endogenous acidic and basic fibroblast growth factors (FGF) participate in ischaemia induced collateral enlargement and development in the myocardium, and also which cells may represent the source of these growth factors. Eight pigs received an ameroid constrictor around the left circumflex coronary artery which, by slow coronary occlusion, induces ischaemia and collateral growth in the left ventricle. The degree of stenosis and development of collaterals were determined angiographically. About 14 d after constrictor implantation pigs were killed and hearts were excised and prepared for western blot analysis and immunohistochemistry. Monoclonal antibodies were raised against acidic and basic FGF, characterised for their specificity, and used for the localisation of growth factors in sections of ischaemic and normal pig heart. The eight pigs included in this study showed a gradual 70-100% left circumflex coronary stenosis about 14 d after implantation of the constrictor. Out of four pigs with a complete occlusion, three developed visible collaterals. Antibody staining to acidic FGF was detected only in hearts from pigs with complete occlusion of the coronary artery. The growth factor was localised in cardiomyocytes close to small necrotic tissue patches. In control tissue no acidic FGF staining was evident. Basic FGF could not be detected in ischaemic or in normal perfused pig hearts. These data show that (1) complete occlusion of the left circumflex coronary artery in pig hearts induces collateral growth; (2) cardiomyocytes are able to produce acidic FGF in response to ischaemia, thus providing a mitogen for endothelial cells; (3) endogenous basic FGF, which was not detected in normal or ischaemic pig hearts, appears not to play an important role in ischaemia induced collateral growth at the chosen time point of investigation.

Prognosis in ischemic heart disease. Can you tell as much at the bedside as in the nuclear laboratory?

BACKGROUND--While the resting left ventricular ejection fraction (LVEF) predicts prognosis in ischemic heart disease, clinical evaluation is also useful. METHODS--To compare the prognostic value of LVEF by resting radionuclide ventriculography with that of clinical signs and symptoms of congestive heart failure (CHF), 170 patients with suspected ischemic heart disease were followed up in this prospective study. Patients had a standardized history and physical examination performed by a study cardiologist immediately before the nuclear scan. Chest roentgenography and radionuclide ventriculography were performed in a standard manner. The diagnosis of CHF was made by validated clinicoradiographic criteria based on the Framingham study. Mortality was determined by means of the National Death Index; median follow-up time was 3 years. RESULTS--There was CHF at baseline in 70 patients, and baseline LVEF was low (< or = 0.4) in 63 patients. Low LVEF was significantly associated with CHF. During follow-up, 55 of the subjects died (overall mortality, 32%). Subjects with CHF had a significantly higher risk of death than those without CHF, and subjects with low LVEF had a higher mortality than those with preserved LVEF. Both CHF and LVEF were independent predictors of mortality. In a Cox model, each percentage increase in LVEF was associated with a 2% decreased mortality, while subjects with CHF had a mortality 2.5 times higher than that of those without CHF. Also, CHF with preserved LVEF had a better prognosis than CHF with depressed LVEF, but this prognosis was worse than that in subjects without CHF. CONCLUSIONS--The clinical diagnosis of CHF, based on clinical evaluation and chest roentgenogram, is a valid predictor of mortality and provides information independent of the radionuclide LVEF in determining prognosis in patients with ischemic heart disease.