Evidence Of Previous Myocardial Infarction Research Articles

P5278Myocardial abnormalities in people living with Human Immunodeficiency Virus (PLWH) detected using cardiovascular magnetic resonance (CMR)

Abstract Background Antiretroviral therapy (ART) has dramatically improved the prognosis in PLWH with survival nearing that of HIV negative people. PLWH may develop significant comorbidities as they age including cardiovascular disease (CVD) such as myocardial infarction, sudden cardiac death, heart failure, as well as subclinical evidence of myocardial inflammation. Overall, ART treated patients are at an increased CVD risk with some studies quoting a 2.2 fold relative risk. Aim To assess the incidence of functional, structural and tissue characterisation changes in PLWH using CMR with multiparametric mapping Methods 39 PLWH (34 men, mean age 55.8±10.9, mean duration of HIV 17.8±9.29 years) and 29 healthy volunteers (20 men, mean age 45.1±8.3) underwent CMR with late gadolinium enhancement (LGE) imaging, T1 and T2 mapping. Results Of PLWH, only 7 scans (18%) were normal. LV ejection fraction was significantly lower and LV mass significantly higher compared to controls. Native T1, a marker of diffuse fibrosis or increased myocardial water content was no different between the groups. T2, a more specific marker of myocardial oedema, was elevated in PLWH. Sixteen PLWH (41%) had evidence of LGE including 8 with an ischaemic pattern (7 sub-endocardial and one transmural) and 8 with a non-ischaemic pattern (5 with mid-wall enhancement and 3 with RV insertion point LGE. No controls had evidence of LGE. Student t-Test: PLWH versus controls PLWH (n=39) Control (n=29) P-value LVEF (%) 59±15 67±5 <0.01 iLVM 79±24 56±13 <0.01 Native T1 (ms) 1021±52 1001±41 0.116 T2 (ms) 48±2 46±2 <0.05 LGE 16 (41%) 0 (0%) <0.001 LVEF (%) = Left Ventricular Ejection Fraction; iLVM = Indexed Left Ventricular Mass (g/m2); LGE = Late Gadolinium Enhancement. Conclusion This study identifies a number of cardiac changes associated with HIV and prolonged treatment with ART. The elevated LV mass may be associated with hypertension, commonly found in PLWH. The elevated myocardial T2 compared to controls may be due to chronic inflammation associated to prolonged HIV exposure. There was no evidence of diffuse fibrosis but focal areas of non-ischaemic scar were a common finding which may relate to previous myocarditis or HIV-related cardiomyopathy. A fifth of PLWH also had evidence of previous myocardial infarction. We propose to image asymptomatic PLWH to further classify, diagnose and treat a vulnerable group of patients who are now described as having a normal life expectancy.

Regional differences of fat depot attenuation using non-contrast, contrast-enhanced, and delayed-enhanced cardiac CT

Regional fat density assessed by computed tomography (CT) has been suggested as a marker of perivascular adipose tissue inflammation. Dual energy CT (DECT) allows improved tissue characterization compared to conventional CT. To explore whether DECT might aid regional fat density discrimination. We included patients who had completed a non-enhanced cardiac CT scan, CT coronary angiography (CTCA), and a delayed enhancement CT. Attenuation levels (Hounsfield units [HU]) were assessed at the epicardial, paracardial, visceral, and subcutaneous fat. The number of coronary segments with disease (SIS) was calculated. A total of 36 patients were included in the analysis. Twenty-six (72%) patients had evidence of obstructive disease at CCTA and 25 (69%) patients had evidence of previous myocardial infarction. At non-contrast CT, we did not identify significant attenuation differences between epicardial, paracardial, subcutaneous, and visceral fat depots (-110.8 ± 9 HU, vs. -113.7 ± 9 HU, vs. -114.7 ± 8 HU, vs. -113.8 ± 11 HU, P = 0.36). Significant attenuation differences were detected between fat depots at mid and low energy levels, both at CTCA and delayed-enhancement scans ( P < 0.05 for all). Epicardial fat showed the least negative attenuation, irrespective of the acquisition mode; epicardial fat evaluated at 40 keV was related to the SIS (r = 0.37, P = 0.03). In this study, regional fat depots amenable to examination during thoracic CT scans have distinctive regional attenuation values. Furthermore, such differences were better displayed using contrast-enhanced monochromatic imaging at low energy levels.

Iodine-123 metaiodobenzylguanidine scintigraphy for the assessment of cardiac sympathetic innervation and the relationship with cardiac autonomic function in healthy adults using standardized methods.

Global iodine-123 metaiodobenzylguanidine (I-MIBG) uptake is predictive of cardiovascular events and mortality in patients with heart failure. Normal variations in global and regional uptake, however, are not well defined and few studies have addressed the functional relevance of I-MIBG uptake and distribution in healthy individuals. We performed I-MIBG scintigraphy and cardiac autonomic function testing using the standardized methodology in 15 healthy individuals (mean age 54.6±5.3 years, male : female 10 : 5) with no evidence of previous myocardial infarction or ischaemic heart disease. Early heart to mediastinum ratio (HMR) was 1.67±0.13, late HMR was 1.73±0.16 and washout rate was 19.09±7.63% (4.20-31.30). Regional analysis showed reduced tracer uptake at the apex, base and inferior wall in all individuals. Early and late HMR correlated negatively with RFa (r=-0.603; P=0.05 and r=-0.644; P=0.033) and expiration and inspiration ratio (r=-0.616; P=0.043 and r=-0.676; P=0.022) and positively with LFa/RFa (r=0.711; P=0.014 and r=0.784; P=0.004). Washout rate correlated only with RFa (r=0.642; P=0.033). Healthy adults show a heterogeneous pattern of cardiac innervation with reduced regional uptake of I-MIBG. Furthermore, HMR correlates with indices of cardiac sympathetic function, suggesting that it might not only be a useful prognostic marker but may also provide insight into the functional integrity of the cardiac autonomic nervous system.

Chronic Total Artery Occlusions in Noninfarct-Related Coronary Arteries

It has been rarely encountered some patients in clinical practice with coronary artery chronic total occlusion (CTO) on angiography but no any clinical history or electrocardiographic, echocardiographic, or left ventriculographic evidence of previous myocardial infarction. These noninfarct-related artery CTO (non-IRA CTO) lesions may be used as a clinical role model of endogenous cardioprotective mechanisms in addition to continuing the process of atherosclerosis. The objective of this study was to characterize the clinical characteristics of patients with non-IRA CTO patients and compared them to those with infarct-related CTO (IRA-CTO). We reviewed our invasive cardiology database searching for the CTO of any major coronary arteries, and assessed whether or not they have the clinical history or electrocardiographic, echocardiographic, and left ventriculographic evidence of previous myocardial infarction. Interestingly, we detected that all these patients with non-IRA CTO had diabetes mellitus, and the clinical and demographic features of these non-IRA CTO patients were compared with age- and sex-matched diabetic IRA-CTO patients with regard to conventional coronary risk factors and the angiographic collateral grading system. There were total 99 CTO patients (49 patients with non-IRA CTO and 50 patients with IRA-CTO).All patients with non-IRA CTO had better collateral circulation (96 vs. 40% p < 0.001) compared with those having IRA-CTO. The only significant difference between the groups was the status of current smoking (4 vs. 88%; p < 0.001). The present study showed that the non-IRA CTOs were associated with diabetes mellitus and better collateral development compared with IRA-CTO. In diabetic patients, the concomitant smoking use may be harmful by preventing endogenous cardioprotective mechanisms.

Abstract 17990: Ectopic Fat is Associated With Gender-specific Reductions in Left Ventricular Myocardial Perfusion Index During Dobutamine Stress

Background: Obesity and visceral adiposity are increasingly recognized risk factors for cardiovascular disease. Visceral fat may reduce myocardial perfusion by impairing endothelial function. Accordingly, we evaluated the association of visceral fat and quantitative myocardial perfusion during peak dose dobutamine stress using MRI. Methods: We evaluated MRI myocardial perfusion index (MPI) in 59 individuals at risk for their first episode of symptomatic heart failure with a left ventricular (LV) ejection fraction &gt;45% and no MRI evidence of previous myocardial infarction or inducible ischemia. MPI was calculated after the first pass of gadolinium (by dividing the upslope of the signal intensity over time curve of the mid LV septum by the upslope of the LV cavity blood curve) after dobutamine and atropine were administered to achieve 80% of the maximum predicted heart rate response for age. Pericardial, subcutaneous (SQ), intraabdominal (IA) and retroperitoneal (RP) fat volumes were quantified using validated MRI techniques. All analyses were blinded to participant identifiers. Pearson’s coefficients were determined and a p-value of &lt; 0.05 was considered significant. Results: Participants averaged 66 ± 7 years in age; 34% were men, 27% African American, 43% diabetic, and 93% were hypertensive. Overall, pericardial, IA, and RP fat were negatively associated with MPI (Table). No fat depots were associated with reduced MPI in men. However pericardial (r=-0.57, p=0.02), IA (r=-0.34, p=0.04) and SQ fat (r=-0.42, p=0.01) were all negatively associated with MPI in women. Conclusions: Higher pericardial, IA and RP fat volumes are associated with reduced LV myocardial perfusion at peak dobutamine stress in women. These findings suggest visceral fat may contribute to abnormal microcirculatory coronary arterial perfusion syndromes, explaining why some women may exhibit more anginal symptoms despite typically lower grade coronary artery stenoses than men.

Resolution of a left ventricular thrombus by the thrombolytic action of dabigatran

A 77-year-old man was referred to our cardiovascular department for detailed examination after abnormal electrocardiography findings were obtained during a preoperative cataract surgery workup. Ultrasound echocardiography (UCG) and computed tomography (CT) revealed evidence of previous myocardial infarction with anteroseptal akinesis and a left ventricular (LV) thrombus (14 × 12 mm). Dabigatran (220 mg/day) was prescribed as an outpatient treatment, and the disappearance of the LV thrombus was confirmed by UCG and CT 27 days after dabigatran initiation. No thromboembolism occurred between treatment initiation and thrombus resolution. Our results indicate that dabigatran has thrombolytic action on an acute pre-existing intracardiac thrombus.

Electrocardiographic Assessment of Coronary Artery Disease and Stroke Risk Factors in Rural and Urban Tanzania: A Case–control Study

BackgroundAlthough the association between cerebrovascular and coronary artery disease (CAD) is well known in high-income countries, this association is not well documented in black Africans.AimsThe aim of this study was to document electrocardiographic (ECG) evidence of CAD in stroke cases and controls and to identify other common ECG abnormalities related to known stroke risk factors in a community-based population of incident stroke cases in Tanzania, East Africa.MethodsThis was a case–control study. Incident stroke cases were identified by the Tanzanian Stroke Incidence Project. Age- and sex-matched controls were randomly selected from the background population. Electrocardiograms were manually analyzed using the Minnesota Coding System, looking for evidence of previous myocardial infarction (MI), atrial fibrillation (AF) or atrial flutter (AFl), and left ventricular hypertrophy (LVH).ResultsIn Hai, there were 93 cases and 241 controls with codable electrocardiograms, and in Dar-es-Salaam, there were 39 cases and 72 controls with codable electrocardiograms. Comparing cases and controls, there was a higher prevalence of MI and AF or AFl (but not LVH) in cases compared with controls.ConclusionsThis is the first published study of ECG assessment of CAD and other stroke risk factors in an incident population of stroke cases in sub-Saharan Africa. It suggests that concomitant CAD in black African stroke cases is more common than previously suggested.

Frequency of Myocardial Infarction and Its Relationship to Angiographic Collateral Flow in Territories Supplied by Chronically Occluded Coronary Arteries

Despite complete interruption of antegrade coronary artery flow in the setting of a chronic total occlusion (CTO), clinical recognition of myocardial infarction is often challenging. Using cardiac MRI, we investigated the frequency and extent of myocardial infarction in patients with CTO, and assessed their relationship with regional systolic function and the extent of angiographic collateral flow. We included 170 consecutive patients (median age, 62 years) with angiographically documented CTO. Regional late gadolinium enhancement and wall motion score index were assessed by cardiac MRI with the use of a 17-segment model. Angiographic collateral flow was assessed by the collateral connection grade and the Rentrop score. Evidence of previous myocardial infarction was found in 25% of patients by ECG Q waves, in 69% by regional wall motion abnormality, and in 86% of patients by late gadolinium enhancement. Increased angiographic collateral flow was associated with a lower frequency of Q waves on ECG, and a lower regional wall motion score index, late gadolinium enhancement volume (%), and degree of late gadolinium enhancement transmurality (all P<0.001), as well. The frequency of myocardial infarction in territories subtended by CTO is significantly higher than previously recognized. The degree of myocardial injury downstream epicardial CTO is inversely correlated with the degree of angiographic collaterals.

Duration of Myocardial Early Systolic Lengthening Predicts the Presence of Significant Coronary Artery Disease

This study sought to investigate whether the duration of left ventricular (LV) early systolic lengthening could accurately identify patients with significant coronary artery disease (CAD). Ischemic myocardium with reduced active force will lengthen when LV pressure rises during early systole before onset of systolic shortening. We included 88 patients with suspected CAD referred to elective diagnostic coronary angiography. Two of these patients were excluded from the study due to evidence of previous myocardial infarction on contrast-enhanced magnetic resonance imaging. Speckle tracking echocardiography was performed before coronary angiography and at follow-up scheduled 1 year after revascularization, and global longitudinal strain and duration of average LV early systolic lengthening were recorded. Forty-three of 86 patients had significant CAD. The duration of early systolic lengthening was significantly prolonged in patients with significant CAD compared with patients without significant coronary artery stenoses (76 ± 37 ms vs. 38 ± 23 ms, p < 0.001). Correspondingly, global systolic strain was significantly lower in patients with CAD (-17.7 ± 3.0% vs. -19.5 ± 2.6%, p = 0.003). Prolonged duration of early systolic lengthening showed the best accuracy in detecting CAD, with an area under the receiver-operating characteristic curve of 0.83. The area under the curve for global strain was 0.68. At 1-year follow-up, the duration of early systolic lengthening was significantly reduced (64 ± 37 ms vs. 76 ± 37 ms, p = 0.041) in the patients treated with revascularization. Duration of myocardial early systolic lengthening was prolonged in patients with significant CAD; this might be a useful parameter to identify patients who might benefit from reperfusion therapy.

Impact of type 2 diabetes and the metabolic syndrome on myocardial structure and microvasculature of men with coronary artery disease

BackgroundType 2 diabetes and the metabolic syndrome are associated with impaired diastolic function and increased heart failure risk. Animal models and autopsy studies of diabetic patients implicate myocardial fibrosis, cardiomyocyte hypertrophy, altered myocardial microvascular structure and advanced glycation end-products (AGEs) in the pathogenesis of diabetic cardiomyopathy. We investigated whether type 2 diabetes and the metabolic syndrome are associated with altered myocardial structure, microvasculature, and expression of AGEs and receptor for AGEs (RAGE) in men with coronary artery disease.MethodsWe performed histological analysis of left ventricular biopsies from 13 control, 10 diabetic and 23 metabolic syndrome men undergoing coronary artery bypass graft surgery who did not have heart failure or atrial fibrillation, had not received loop diuretic therapy, and did not have evidence of previous myocardial infarction.ResultsAll three patient groups had similar extent of coronary artery disease and clinical characteristics, apart from differences in metabolic parameters. Diabetic and metabolic syndrome patients had higher pulmonary capillary wedge pressure than controls, and diabetic patients had reduced mitral diastolic peak velocity of the septal mitral annulus (E'), consistent with impaired diastolic function. Neither diabetic nor metabolic syndrome patients had increased myocardial interstitial fibrosis (picrosirius red), or increased immunostaining for collagen I and III, the AGE Nε-(carboxymethyl)lysine, or RAGE. Cardiomyocyte width, capillary length density, diffusion radius, and arteriolar dimensions did not differ between the three patient groups, whereas diabetic and metabolic syndrome patients had reduced perivascular fibrosis.ConclusionsImpaired diastolic function of type 2 diabetic and metabolic syndrome patients was not dependent on increased myocardial fibrosis, cardiomyocyte hypertrophy, alteration of the myocardial microvascular structure, or increased myocardial expression of Nε-(carboxymethyl)lysine or RAGE. These findings suggest that the increased myocardial fibrosis and AGE expression, cardiomyocyte hypertrophy, and altered microvasculature structure described in diabetic heart disease were a consequence, rather than an initiating cause, of cardiac dysfunction.

Leukocyte telomere shortening in elderly Type2DM patients with previous myocardial infarction

Objective We performed a cross-sectional study to examine the differences in leukocyte telomere length among three groups of subjects: patients with type 2 diabetes mellitus without history of previous myocardial infarction (Type2DM), patients with type 2 diabetes mellitus with evidence of previous myocardial infarction (Type2DM + MI), and healthy control subjects (CTR). The main objective of the present study is to investigate differences in telomere length between the studied groups of subjects, with the aim to clarify if telomere length could be a reliable marker associated with MI in Type2DM patients. Secondary end point is the identification of associations between leukocyte telomere length and selected variables related to glycemic control, pro-inflammatory status and lipidic profile. Research design and methods A total of 272 elderly subjects, 103 Type2DM (mean age 70 ± 4 years, 59% males), 65 Type2DM + MI (mean age 68 ± 7 years, 68% males), and 104 CTR (mean age 69 ± 7 years, 50% males) were studied. Telomere length, defined as T/S (Telomere-Single copy gene ratio), was determined in leukocytes by quantitative real-time polymerase chain reaction (real-time PCR)-based assay. Moreover, we assessed: (1) high sensitive C reactive protein (hsCRP), fibrinogen and plasminogen-activator inibitor-1 (PAI-1) as inflammatory markers; (2) fasting glucose, insulin, glycated haemoglobin (HbA1C) and waist-to-hip ratio as markers of glycemic control; (3) total-cholesterol, HDL-cholesterol and triglycerides as markers of lipidic profile, in all sample population. The use of statins and sulfonylurea, as well as the presence of some relevant diabetes complications (nephropathy and retinopathy) were also assessed. Conclusion Type2DM + MI elderly patients have leukocyte telomere lengths shorter than those of Type2DM (without MI) and healthy CTR. Moreover, glucose, HbA1C and waist-to-hip ratio, variables related to glycemic control, showed a significant inverse correlation with leukocyte telomeres length.

Clinical Significance of Abnormal Electrocardiographic Findings in Individuals Aging With Spinal Injury and Abnormal Lipid Profiles

Background: Cardiovascular risk factors are common in individuals with chronic spinal cord injury (SCI), and their prevalence increases with age. The actual prevalence of overt cardiovascular disease (CVD) in this population has not been well established.Methods: Electrocardiograms (ECGs) were examined for abnormalities in 43 individuals with abnormal lipid profiles being followed in the outpatient SCI clinic of our institution. The mean age of the study population of predominantly men was 43 ± 9.9 years and the mean duration of injury 16.6 ± 8 years.Results: ECG abnormalities were common and present in 60.5% of participants. ST-T wave abnormalities were the most commonly observed (35%). Evidence of previous myocardial infarction was present in 7% of all individuals and in 12% of those with ECG abnormalities. The only clinical parameter differentiating the group with normal vs abnormal ECG was the duration of injury (19.5 ± 8 y vs 12 ± 5 y; P= 0.0026). Analysis of variance showed that injury duration was the sole predictor of abnormal ECG with 68% accuracy (P = 0.006). Among those with ECG abnormalities, although no significant differences were detected between those with and without evidence of previous myocardial infarction, mean total cholesterol and low-density lipoprotein were higher, and mean high-density lipoprotein was lower. Mean age and injury duration were greater in those with evidence of previous myocardial infarction.Conclusion: Although age is an important risk factor for CVD in the population of individuals without disabilities, injury duration is at least as important as age in those with SCI. Our findings support the recommendation that individuals with SCI and abnormal lipids should be screened for CVD regardless of age.

Plasma homocysteine and oxidative stress in cardiovascular disease.

Hyperhomocysteinemia (Hhcy) has been associated with pathological and stressfull conditions and is a risk factor for cardiovascular disease (CVD). The aim of this study was to evaluate the correlation between plasma homocysteine (hcy) and lipid peroxidation in patient with CVD. This study was carried out on 40 patients with CVD as well as 15 healthy volunteers of comparable age and gender as control group. The patients were divided into 2 groups as follows: group I, included 20 patients with acute myocardial infarction and group II, included 20 patients with atherosclerotic coronary artery disease with no evidence of previous myocardial infarction . Plasma hcy, nitric oxide (NO) and malondialdhyde (MDA) [as index of lipid peroxidation] were measured in all groups. In addition serum total-cholesterol, HDL, LDL and triglycerides were evaluated. Results obtained showed that, there was a significant elevation in the levels of plasma hcy, NO and MDA in groups I and II as compared to control group. There was a strong positive correlation between plasma hcy and MDA (r = 0.59, p < 0.001). Also NO was positively correlated with both hcy (r = 0.49, p < 0.001) and MDA (r = 0.51, p < 0.001) . Serum total cholesterol, LDL, and triglycerids were also significantly elevated while serum HDL was significantly decreased in groups I and II as compared to control group. It can be concluded that, hyperhomocysteinemia is a possible factor in free radical generation and therefore cardiovascular diseases.

Revascularization improves survival in ischemic cardiomyopathy regardless of electrocardiographic criteria for prior small-to-medium myocardial infarcts

Background The purpose of the current study was to determine whether survival after revascularization (coronary artery bypass grafting or percutaneous transluminal coronary angioplasty) is influenced by the extent of electrocardiographic (ECG) evidence of previous myocardial infarction (MI) in patients with ischemic cardiomyopathy by use of the 50-criteria, 31-point Selvester QRS scoring system. Methods Patients with ischemic cardiomyopathy documented by a left ventricular ejection fraction (LVEF) ≤30% undergoing coronary angiography between January 1984 and July 1996, with no acute MI within the last 30 days, follow-up through 1996, and ≥75% occlusion in at least 1 major coronary artery at catheterization were included. These patients were subdivided on the basis of subsequent treatment: revascularization or no revascularization. The complete Selvester QRS system was applied to each patient's ECG and the subgroups were further subdivided by QRS score. Results The 141 patients receiving revascularization had better survival at 5 years compared with the 298 patients receiving no revascularization (adjusted 5-year survival rate 73% vs 47%, P =.0001). No significant treatment differences were observed for low (≤3 points) versus high (>3 points) QRS levels in either of the 2 treatment groups (revascularized patients: P =.215, patients without revascularization: P =.126) between the 2 treatment groups. Although all patients had LVEF ≤30%, only 8% of patients had QRS scores >10 points, the level that would be expected if the decrease in LVEF could be attributed entirely to infarcted myocardium. Conclusions Hibernating myocardium may contribute significantly to the decreased function in patients with ischemic cardiomyopathy, and the QRS score cannot be used as an independent predictor of survival in those patients with a marked decrease in LVEF but small to moderate infarct sizes. (Am Heart J 2002;143:111-7.)

Ischemic heart disease in black South African stroke patients.

Stroke patients in western countries frequently have coronary artery disease (CAD). In black Africans, CAD has been reported as being rare in both stroke patients and the general population. In this study, an attempt has been made to determine the prevalence of CAD in a black South African stroke population. The prevalence of CAD was determined by indicators identified through a series of 5 observational studies in black patients diagnosed with stroke. CAD indicators included (1) bedside diagnosis in 741 patients; (2) resting ECG in 555 consecutively admitted patients; (3) a combination of clinical examination, cardiac ultrasound, radionuclide scintigraphy, and multigated blood pool studies in 102 consecutively admitted patients; (4) thallium scintigraphy in 60 patients; and (5) necropsy in 23 patients. On bedside questioning, only 0.7% complained of previous angina. There was no history given of myocardial infarction (MI), but documentation of this was found in the clinical notes of 0.7% of the patients. In the resting ECG study, evidence of myocardial ischemia was present in 14.6% and MI in 2.1%. In the combined study, cardiac ischemia was documented on ECG in 12.7% of patients and evidence of previous MI in 5.8%. Cardiac scintigraphic studies revealed changes of myocardial ischemia in 31.7% and MI in 13.3% of the 60 patients studied. Four (17.4%) of 23 patients in the necropsy study had histological evidence of previous MI, and 50% of all patients had evidence of >50% atherosclerotic stenosis in 1, 2, or 3 coronary arteries. The prevalence of CAD in black African stroke patients is significantly higher than has been documented in the general nonstroke black population as well as in stroke patients. Black stroke patients may have a risk for CAD similar to that of their white counterparts.

Global biventricular dysfunction in patients with asymptomatic coronary artery disease may be caused by myocarditis.

The causal role of asymptomatic critical coronary artery obstruction in patients presenting with severe global biventricular dysfunction but no evidence of myocardial infarction is uncertain. Among 291 patients aged >40 years undergoing a noninvasive (2-dimensional echocardiography) and invasive (catheterization, coronary angiography, and biventricular endomyocardial biopsy, 6 to 8 samples/patient) cardiac study because of progressive heart failure (New York Heart Association functional class III or IV) with global biventricular dysfunction and no history of myocardial ischemic events, 7 patients (2.4%; 7 men; mean age, 49+/-6.9 years) had severe coronary artery disease (3 vessels in 4 patients; 2 vessels in 1 patient, proximal occlusion of left anterior descending coronary artery in 2 patients). Left ventricular end-diastolic diameter and ejection fraction by 2-dimensional echocardiography were 73+/-10.5 mm and 23+/-6.5%, respectively, and right ventricular end-diastolic diameter and ejection fraction were 39+/-7 mm and 29+/-7.2%, respectively. Biopsy specimens showed extensive lymphocytic infiltrates with focal myocytolysis meeting the Dallas criteria for myocarditis in all patients (in 5 patients with and 2 patients without fibrosis). Cardiac autoantibodies were detected with indirect immunofluorescence in the serum of 2 patients with active myocarditis. The 2 patients with active inflammation received prednisone (1 mg. kg-1. d-1 for 4 weeks followed by 0.33 mg. kg-1. d-1 for 5 months) and azathioprine (2 mg. kg-1. d-1 for 5 months) in addition to conventional drug therapy for heart failure. At 8-month overall follow-up, cardiac volume and function improved considerably in immunosuppressed patients but remained unchanged in conventionally treated patients, of whom 1 died. Global biventricular dysfunction in patients with severe asymptomatic coronary artery disease and no evidence of previous myocardial infarction may be caused by myocarditis. Histologic findings may influence the treatment.

A comparison of coronary artery bypass grafting and percutaneous transluminal coronary angioplasty in patients on hemodialysis

The hospital records of 22 patients on hemodialysis undergoing coronary artery bypass grafting, and 19 others undergoing percutaneous transluminal coronary angioplasty were reviewed to compare the outcomes of these procedures in this population. Evidence of previous myocardial infarction or triple vessel or left main coronary artery disease was more common in patients undergoing coronary artery bypass graft than those undergoing percutaneous transluminal coronary angioplasty. Perioperative mortality and complication rates following coronary artery bypass graft (4.5% and 41%, respectively) were similar to those following percutaneous transluminal coronary angioplasty (5.3% and 42%). Cardiac event-free rates at 18 months by life-table analysis following coronary artery bypass graft and percutaneous transluminal coronary angioplasty were 87±16% and 40±14%, respectively. Survival at 18 months were 67±17% following coronary artery bypass graft and 69±14% following percutaneous transluminal coronary angioplasty. Cardiac events were observed to occur in three patients undergoing coronary artery bypass graft at a median of 10 months, and in nine patients following percutaneous transluminal coronary angioplasty at a median of 6 months. One patient required percutaneous transluminal coronary angioplasty after the initial coronary artery bypass graft. Seven patients required repeat percutaneous transluminal coronary angioplasty, and two patients underwent coronary artery bypass graft after initial percutaneous transluminal coronary angioplasty. Although these conclusions are limited by the retrospective nature of the study, it is concluded that coronary artery bypass graft can be performed with morbidity and mortality equivalent to percutaneous transluminal coronary angioplasty, and provides better cardiac event-free rates than percutaneous transluminal coronary angioplasty in patients on hemodialysis. Percutaneous transluminal angioplasty does not appear to be justified in this population because of its unacceptably high restenosis and cardiac event rates.

Chronic heart failure in the United States: a manifestation of coronary artery disease.

failure were a homogeneous disease process, regardless of whether patients had underlying CAD. The main enrollment criterion in most clinical trials was, and continues to be, symptoms of congestion and/or evidence of LV systolic dysfunction. The diagnosis of CAD, the leading cause of heart failure in these studies, has often been based on subjective evidence such as history of angina pectoris and has not always required definitive criteria, such as objective evidence of previous myocardial infarction, significant obstructive CAD on coronary arteriography, or evidence of inducible myocardial ischemia. Thus, the true prevalence of CAD, and its contribution to LV dysfunction, may be higher than actually reported in many of the trials. It follows that the efficacy or lack of efficacy of the heart failure agents under investigation in these trials is difficult to determine in patients with CAD. In addition, the possibility of progression of CAD during the study period has not been assessed, nor has the possibility that mortality in many patients with heart failure may be related more to the progression of CAD than to the progression of LV

Chronic myocardial hibernation in humans. From bedside to bench.

Since the pioneering work of Tennant and Wiggers,1 it has been known that total ischemia leads to a prompt cessation of contraction and eventually results in the appearance of cell damage and irreversible myocardial necrosis. Accordingly, in the minds of many cardiologists, the discovery of an abnormal regional contraction in a patient with coronary artery disease has long been equated with the presence of irreversible myocardial necrosis. With the advent of recanalization therapy, however, evidence progressively accumulated that prolonged regional “ischemic” dysfunction did not always arise from irreversible tissue damage and, to some extent, could be reversed by restoration of blood flow.2 3 4 5 These observations have led to the speculation that chronically hypoperfused myocardium, which is often referred to as “hibernating,”2 3 4 5 6 could maintain viability by simply reducing its metabolic demand to match the decreased supply for as long as myocardial perfusion was inadequate. The chronic impairment of contractile function in this setting has been regarded as a protective mechanism by which the heart spontaneously downgrades its myocardial function, minimizes its energy requirements, and prevents the appearance of irreversible tissue damage.2 4 5 The concept of chronic hibernation thus consists of two parts: a unique clinical observation that bears important implications for the management of patients with chronic coronary artery disease2 3 4 5 6 and a pathophysiological hypothesis, yet to be demonstrated, implying that the chronic dysfunction is due to a chronic reduction of resting MBF.4 5 Other aspects that were not included in the original description, ie, the rapidity of mechanical recovery after successful revascularization7 and the response of dysfunctional myocardium to inotropic stimulation, are now also considered to be integral parts of this condition. The purpose of this discussion is to review some of the …

Diet-heart issues in a pharmacological era

Reduction of serum cholesterol low-density lipoprotein (LDL) is an important step in secondary and primary prevention of coronary heart disease, and clinical trials have now shown that cholesterol lowering drugs substantially lessen coronary risk within a few years? These findings will undoubtedly increase the popularity of cholesterol lowering by drugs at the expense of dietary modification. However, properly applied dietary changes should be the first step in cholesterol lowering. In this short overview I focus on two elements of a healthy-heart diet--fatty acids and antioxidants. Fatty acids are a major determinant of serum cholesterol and LDL concentrations. Antioxidants may prevent oxidative modification of LDL, which is an important step in the development of atherosclerosis. I also discuss the effectiveness of dietary intervention.