Course Of Ischemic Heart Disease Research Articles

COMPLICATED COURSE OF ISCHEMIC HEART DISEASE IN A PATIENT WITH OBSTRUCTIVE SLEEP APNEA

Obstructive sleep apnea (OSA) can activate pathological routes which can lead to insulin resistance, development of atherosclerosis and hypertension. The combination of hypertension and OSA has an additive effect on the development of atherosclerosis. As a number of studies have revealed, that the incidence of OSA in patients with myocardial infarction is likely to be high. We present a patient with acute myocardial infarction and no classical coronary artery disease risk factors: non-smoker, normal blood pressure, normal total and low-density lipoprotein cholesterol levels, borderline high-density lipoprotein cholesterol level, with good physical activity, no diabetes mellitus, no abdominal obesity, a negative family history. The only risk factor was untreated obstructive sleep apnea. The course of disease was complicated by subsequent in-stent restenosis and progression of atherosclerotic plaques, which led to the need for acute coronary artery bypass graft surgery complicated by consecutive in-anastomosis stenosis despite maximum cardiovascular therapy. One year of continuous positive airway pressure treatment was needed to stabilize his health condition, which is now stable for up to two years. Given the complicated course of ischemic heart disease in patients with OSA, we believe that OSA diagnosis would be advisable each time these patients with symptoms of myocardial infarction, ischemic heart disease and OSA are examined. Even more important, however, is proper treatment of the OSA when it is present.

EFFECT OF FERROTHERAPY ON COURSE OF ISCHEMIC HEART DISEASE ASSOCIATED WITH MILD IRON DEFICIENCY IN MEN

Aim. To assess effect of ferrotherapy on course of ischemic heart disease (IHD) associated with mild iron deficiency anemia (IDA) and latent iron deficiency (ID). Material and methods. 80 male patients, coal miners, aged 51±7.9 years, were observed. 28 patients had angina pectoris associated with the mild IDA, 23 patients experienced myocardial infarction accompanied by the mild IDA and 29 patients had angina with latent ID. Latent ID was defined in case of iron plasma level ≤12 µg/l, IDA was diagnosed in case of hemoglobin level <130 mg/l. The minimal hemoglobin level observed in patients was 107g/l. ICD clinical characteristics were compared before and after 3-week iron-based treatment in individualized doses. Results. Latent ID and mild IDA aggravated angina and increased ectopic myocardial activity in patients with IHD. Iron-based therapy with appropriate nutrition reduced angina attacks frequency, duration and intensity, decreased nitroglycerin consumption and increased exercise tolerance. Conclusion. Normalization of haemoglobin level and iron plasma concentration in the mild IDA as well as normalization of iron plasma concentration in ID in patients with IHD reduces ede-ma and dyspnea, decreases heart rate. These effects are provided due to the treatment with elementary iron in individualized course dose, which improves clinical status and minimizes the adverse reactions.

Cardiomyocyte remodeling in ischemic heart disease

The aim of the study was to detect changes in left ventricular cardiomyocyte size and shape in response to chronic ischemia and loss of cardiac tissue (myocardial infarction) during the course of ischemic heart disease (IHD). Left ventricular cardiomyocyte dimensions (diameter and length) were estimated histomorphometrically, and their cross-sectional area and volume were assessed in 85 males who died suddenly out of hospital (within 6 hours of the onset of the terminal event) due to the acute first (preinfarction IHD group, n=53, aged 48.6+/-2.9 years) or repeated (postinfarction IHD group, n=32, aged 51.7+/-2.9 years) IHD attack, and had no other causes for the increased heart load. Twenty-nine males of similar age (mean age, 46.0+/-3.1 years) who succumbed to external causes served as controls. We have found cardiomyocyte hypertrophy in the preinfarction IHD group already. The cardiomyocyte volume was increased by 32.0% in comparison with the same index in the control group, and cross-sectional area and length--by 17.2 and 12.5%, respectively. In postinfarction IHD group, all studied cardiomyocyte parameters did not differ significantly from the analogous indices in the preinfarction IHD group (P>0.05). Cardiomyocyte hypertrophy was related to the increase in left ventricular cardiomyocyte parameters. Left ventricular cardiomyocyte hypertrophy occurs before the first myocardial infarction. In postinfarction myocardium, cardiomyocyte dimensions do not differ significantly at least prior to the appearance of congestive heart failure syndrome.

EFFICACY AND SAFETY OF METOPROLOL SUCCINATE IN HIGH DOSES IN PATIENTS WITH STABLE COURSE OF ISCHEMIC HEART DISEASE

Aim. To compare two initial doses (50 or 100mg/day) ofmetoprolol succinate in control released presentation (Betaloc ZOK, AstraZeneca) for achievement of target level of heart rate (HR) in patients with stable course of ischemic heart disease (IHD). Material and methods. 50 patients (34 men and 16 women, aged 61,3 y.o., in average) with IHD were involved into the open randomized comparative study. IHD duration was from 1 to 22 years (8,3 years in average). 47 patients completed study, 3 patients drop out because of side effects. Previous therapy with β-blockers or other HR reducing drugs was replaced on metoprolol. Patients were randomized in 2 groups (G1 and G2). The initial metoprolol dose was 50 mg in G1 patients and 100 mg - in G2 patients. The dose was enlarged twice if necessary. Study duration was 6 weeks. The change of HR, blood pressure, electrocardiogram parameters was evaluated. Patients filled in Seattle angina questionnaire initially and after 6 weeks treatment. Therapy tolerability was also estimated. Results. In 6 weeks of therapy 61% of G1 patients and 87,5% of G2 patients (p<0,01) reached HR target. Dependence of achievement of target HR and dose of metoprolol was observed (r=0,3; p=0,056). Improvement of the HR control was accompanied by reduction of frequency of angina attacks and increase of life quality. Conclusion. Metoprolol (Betaloc ZOK) 200 mg/day provides more effective HR control in patients with IHD vs metoprolol 50-100 mg/day and has good tolerability.

IMMUNO-INFLAMATORY RESPONSES IN ACUTE CORONARY SYNDROME

Aim. To determine the role of immuno-inflammatory responses in the development of acute coronary syndrome (ACS). Material and methods. 93 patients with acute coronary syndrome (ACS), including 60 patients with unstable angina (UA) and 33 patients with acute myocardial infarction (AMI) were involved in the study. Comparison group included 83 patients with stable angina and control group - 25 healthy persons. The diagnosis of ischemic heart disease (IHD) was verified on the basis of clinical and instrumental data. For assessment of immuno-inflammatory responses levels of C-reactive protein (CRP), pro-inflammatory (interleukins [IL-1β, IL-6], tumor necrosis factor [TNF-α]) and anti-inflammatory (IL-4, IL-10) cytokines we determined by ELISA method. Results. There were high levels of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α), high CRP level and low levels of anti-inflammatory IL-4, IL-10 cytokines in UA and AMI patients. Insignificant immunological shifts were found in stable angina patients. Conclusion. Destabilization in the IHD course is characterized with more active immuno-inflammatory responses. Activity of these reactions is asso???ciated with ACS severity.

IMMUNO-INFLAMATORY RESPONSES IN ACUTE CORONARY SYNDROME

Aim. To determine the role of immuno-inflammatory responses in the development of acute coronary syndrome (ACS). Material and methods. 93 patients with acute coronary syndrome (ACS), including 60 patients with unstable angina (UA) and 33 patients with acute myocardial infarction (AMI) were involved in the study. Comparison group included 83 patients with stable angina and control group - 25 healthy persons. The diagnosis of ischemic heart disease (IHD) was verified on the basis of clinical and instrumental data. For assessment of immuno-inflammatory responses levels of C-reactive protein (CRP), pro-inflammatory (interleukins [IL-1β, IL-6], tumor necrosis factor [TNF-α]) and anti-inflammatory (IL-4, IL-10) cytokines we determined by ELISA method. Results. There were high levels of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α), high CRP level and low levels of anti-inflammatory IL-4, IL-10 cytokines in UA and AMI patients. Insignificant immunological shifts were found in stable angina patients. Conclusion. Destabilization in the IHD course is characterized with more active immuno-inflammatory responses. Activity of these reactions is asso￾ciated with ACS severity.

EFFECTS OF ENALAPRIL ON ENDOTHELIUM FUNCTION IN PATIENTS WITH ISCHEMIC HEART DISEASE

Aim. To study endothelium vasomotor function (EF) in patients with ischemic heart disease (IHD) and the influence of angiotensin converting enzyme inhibitor enalapril (Enam, Dr .Reddy’s, India) on it. Material and methods. 87 patients were examined totally. 49 patients were suffering from IHD: 18 patients were younger than 60 years old and 31 patients were older . The combination of arterial hypertension (HT) and IHD were registered in 38 patients: 18 patients were below and 20 patients were above 60 years old. All patients additionally to basic IHD therapy took enalapril in dose 2,5-30 mg/daily during 12 weeks. Before the beginning and in the end of treatment cuff test, test with nitroglycerine, bicycle exercise test and Holter monitoring were made, the thickness of intima-media complex of carotid artery and the level of endothelin-1 in blood plasma were defined. Results. EF disorders were shown in IHD, maximal disorders were determined in patients with combination of IHD and HT. EF disorders were also more expressive in patients of elder group. Enalapril restored of cuff tests results, nitroglycerine tests results, reduced a number of myocardial ischemia episodes and provided target blood pressure in 60, 5% patients with HT. Conclusion. Enalapril improves endothelium vasomotor function, endothelium reaction on nitroglycerine and clinical course of IHD and HT.

The role of neutrophils in destruction of vascular endothelium in myocardial revascularization surgeries under extracorporeal circulation

Aimed at studying endothelial destruction dependence on functional activity of neutrophils, 42 patients with ischemic heart disease (IHD) were examined before, 6 and 24 hours after coronary artery bypass grafting (CABG) under extracorporeal circulation. Level of active forms of oxygen (AFO) in blood neutrophiles, their receptor apparatus (CD18-, Fcg- and C3b-receptors), degranulation and desquamation expression of endothelium were estimated. Clinical course of IHD was shown to be accompanied by the stimulation of AFO production by neutrophils as well as cellular digestion ability, by depression of neutrophils receptors expression and marked endothelial destruction. After CABG, the revealed disorders aggravated, degranulation of neutrophils was noted. Interrelation between neutrophils’ AFO production and endothelial alteration was observed only 6 hours after the surgery.

Treating depression in patients with chronic disease: recognition and treatment are crucial; depression worsens the course of a chronic illness.

see also p 332 Recognition and treatment are crucial; depression worsens the course of a chronic illness Chronic medical illness is consistently associated with an increased prevalence of depressive symptoms and disorders.1,2 In some cases, depression appears to result from specific biologic effects of chronic medical illness. Examples of this relationship include central nervous system disorders—such as Parkinson's disease, cerebrovascular disease, or multiple sclerosis—as well as endocrine disorders—such as hypothyroidism. In other cases, the association between depression and chronic medical illness appears to be mediated by behavioral mechanisms; the limitations on activity imposed by the illness lead to gradual withdrawal from rewarding activities.3 Why should primary care physicians be alert to the possibility of depression in their patients with chronic disease? Why do they sometimes miss it? And what can they do to manage this distressing mental health problem? Depression significantly increases the overall burden of illness in patients with chronic medical conditions. Compared with those without depression, medical outpatients with depressive symptoms or disorders experienced decrements in quality of life4 and had almost twice as many days of restricted activity or missed work because of illness.5 Similarly, depression is associated with a 50% to 100% increase in health services use and costs.6 Depression has also been linked to increased disease-related morbidity and mortality. Results of population-based studies have shown a modest association between depression and all-cause mortality and a stronger association between depression and mortality resulting from cardiovascular disease.7 Depression is clearly associated with a poorer prognosis and more rapid progression of chronic illnesses, including ischemic heart disease8 and diabetes.9 Here as well, the interaction between depression and chronic medical illness may be mediated by either biologic or behavioral mechanisms. For example, depression may affect the course of ischemic heart disease through increased platelet activation or of diabetes through decreased glucose tolerance. It may also affect these diseases by decreasing treatment adherence and physical activity and by increasing tobacco and alcohol use.10 The presence of a chronic medical illness may reduce the likelihood that physicians or other health care providers recognize or treat depression. The demands of chronic illness management may crowd concerns of depression out of the visit agenda. Providers may also not look beyond a chronic medical illness to explain nonspecific symptoms, such as fatigue or poor concentration. Even when they recognize symptoms of depression, they may defer treatment, believing that “anyone would be depressed” in such a situation. Yet, somatic symptoms often reflect a combination of medical and psychological factors, and the presence of a clear medical explanation for these symptoms does not rule out depression as a contributing factor.11 Patients should receive appropriate treatment regardless of whether there is an obvious medical or psychological precipitant to their depression. Because the symptoms of depression—such as fatigue or changes in appetite—may overlap with manifestations of the medical illness, using standard screening tools or diagnostic criteria for depression in patients with chronic disease may lead to overdiagnosis of depression. This concern has led to the development of depression measures, such as the Geriatric Depression Scale,12 that include fewer somatic symptoms. However, it seems that underdiagnosis of depression is a more important problem than is overdiagnosis. Concern about the accuracy of screening or diagnostic measures should not interfere with efforts to improve access to appropriate treatment. So what is the appropriate treatment? First, consider whether a medical problem or medication is causing the depressive symptoms; treating the problem or changing the medication may alleviate the symptoms. Chronic illnesses known to mimic depression include sleep apnea, thyroid disorders, and Cushing's syndrome. Among medical outpatients, however, the prevalence of major depression (6%-10%) is greater than that of “medical mimics” of depression. Exhaustive efforts to rule out medical disorders can delay needed treatment and reinforce the stigmatization of depression as something less than a “real” illness. Second, recognize that randomized trials have shown the efficacy of both pharmacologic13,14,15 and psychosocial16 treatments of depression across a range of chronic medical conditions. Effective treatment of depression reduces depressive symptoms and improves daily functioning. Treating depression has also been shown to have a positive effect on biologic indicators of disease severity or progression, such as the level of glycosylated hemoglobin in diabetes15 or platelet activation in ischemic heart disease.17 Given the clear benefits of recognizing and treating depression, all those who care for people with chronic medical illness should consider identification and treatment of depression a clinical priority.

Beneficial effect(s) of n-3 fatty acids in cardiovascular diseases: but, why and how?

Low rates of coronary heart disease was found in Greenland Eskimos and Japanese who are exposed to a diet rich in fish oil. Suggested mechanisms for this cardio-protective effect focused on the effects of n-3 fatty acids on eicosanoid metabolism, inflammation, β oxidation, endothelial dysfunction, cytokine growth factors, and gene expression of adhesion molecules; But, none of these mechanisms could adequately explain the beneficial actions of n-3 fatty acids. One attractive suggestion is a direct cardiac effect of n-3 fatty acids on arrhythmogenesis. N-3 fatty acids can modify Na+channels by directly binding to the channel proteins and thus, prevent ischemia-induced ventricular fibrillation and sudden cardiac death. Though this is an attractive explanation, there could be other actions as well. N-3 fatty acids can inhibit the synthesis and release of pro-inflammatory cytokines such as tumor necrosis factorα (TNFα) and interleukin-1 (IL-1) and IL-2 that are released during the early course of ischemic heart disease. These cytokines decrease myocardial contractility and induce myocardial damage, enhance the production of free radicals, which can also suppress myocardial function. Further, n-3 fatty acids can increase parasympathetic tone leading to an increase in heart rate variability and thus, protect the myocardium against ventricular arrhythmias. Increased parasympathetic tone and acetylcholine, the principle vagal neurotransmitter, significantly attenuate the release of TNF, IL-1β, IL-6 and IL-18. Exercise enhances parasympathetic tone, and the production of anti-inflammatory cytokine IL-10 which may explain the beneficial action of exercise in the prevention of cardiovascular diseases and diabetes mellitus. TNFα has neurotoxic actions, where as n-3 fatty acids are potent neuroprotectors and brain is rich in these fatty acids. Based on this, it is suggested that the principle mechanism of cardioprotective and neuroprotective action(s) of n-3 fatty acids can be due to the suppression of TNFα and IL synthesis and release, modulation of hypothalamic-pituitary-adrenal anti-inflammatory responses, and an increase in acetylcholine release, the vagal neurotransmitter. Thus, there appears to be a close interaction between the central nervous system, endocrine organs, cytokines, exercise, and dietary n-3 fatty acids. This may explain why these fatty acids could be of benefit in the management of conditions such as septicemia and septic shock, Alzheimer's disease, Parkinson's disease, inflammatory bowel diseases, diabetes mellitus, essential hypertension and atherosclerosis.

Peculiarities of ischemic heart disease course in combination with essential hypertension.

Peculiarities of ischemic heart disease course in combination with essential hypertension.

Myocardial ischemia in Kawasaki disease: Follow-up study by cardiac catheterization and coronary angiography

The clinical course of ischemic heart disease due to Kawasaki disease was analyzed. The subjects (children aged two months to eight years) were divided into two groups. Group 1 (n = 23) consisted of children who had sustained myocardial infarction (MI) and group 2 (n = 13) of those without clinical symptoms or signs of MI, but in whom signs of an obstructive lesion had appeared on coronary arteriography during the follow-up period. Changes in the left ventricular ejection fraction (LVEF) and the appearance of coronary arterial lesions on first and second angiography were analyzed in the two groups. It was found that (a) LVEF (51.4 +/- 13.4%, mean +/- SD) at the first study, obtained after MI in group 1, was significantly lower than that (64.3 +/- 3.7%) at the second one in group 2, which revealed recently developed obstructive lesions; (b) there was no significant difference between the two groups as to the severity of stenotic lesions on coronary arteriography; and (c) comparison of LVEF at the first angiography with that at the second study showed significant improvement in group 1 (1st, 54.2 +/- 12.0%; and 2nd, 60.8 +/- 9.7%) and significant depression in group 2 (1st, 68.1 +/- 4.4%; and 2nd, 64.3 +/- 3.7%).

Treatment of Ischemic Heart Disease

To the Editor.— Ornish et al have described a project that investigated the effect of stress control and dietary changes on the course of ischemic heart disease. They reported a remarkable 91% decrease in anginal episodes and 55% increase in work performance after 24 days in a controlled environment. Their intent was commendable, but the report's value is limited by the number of uncontrolled variables and the fact that some elements of their program are not sustainable over time by most of our population. One planned intervention was a vegan diet averaging 1,400 calories daily. It caused a mean weight loss of 0.19 kg/day (0.42 lb/day) in the experimental subjects, while the weight of the control subjects remained constant. One might believe that weight loss of this magnitude introduces a variable in addition to the types of foods permitted, although the authors state that their statistical analysis indicates otherwise. The

Transient ST segment elevation occurring without anginal pain. Correlations with Prinzmetal's angina

Two cases presenting with episodes of marked ST segment elevation occurring with, but most often without, anginal pain are reported. The changes were recorded through continuous ECG monitoring during Prinzmetal's angina and in the course of myocardial infarction. Such transient asymptomatic ECG abnormalities reveal silent acute myocardial ischemia and are often unrecognized. However, they may lead to severe arrhythmias or myocardial infarction, and sudden deaths occurring in the course of ischemic heart disease are likely to be explained on this basis. Transient episodes of silent ST segment elevation similar to those occurring in Prinztal's angina have been reported in various circumstances. They bring into discussion the delimitations of variant angina pectoris.

Thrombocytopenia and Myocardial Ischemia

Two patients had myocardial ischemia in a setting of chronic thrombocytopenia. Awareness of such occurrences should stimulate the reporting of other cases, so that the role of quantitative changes in platelets on the course of ischemic heart disease may receive greater attention. (<i>JAMA</i>228:1568-1569, 1974)

Transient Abnormal Q Waves in the Course of Ischemic Heart Disease

The significance of transient abnormal Q waves (TAQW) observed during acute coronary insufficiency was studied in 15 patients with atherosclerotic heart disease. TAQW occurred during anginal chest pain (10 of 15), cardiogenic shock (3 of 15) and paroxysmal dyspnea (2 of 15). The anterior myocardial wall was more frequently involved (13 of 15) than the diaphragmatic wall (2 of 15). Serum enzyme levels were normal or slightly increased in 11 of 15. TAQW disappeared in four hours to nine days (mean three days). Three patients died and an autopsy was performed on two of them. It is concluded that cases with TAQW include: (1) acute episodes of myocardial ischemia, without myocardial infarction (MI) (8 of 15); (2) MI with early electrical recovery due to predominant ischemia (4 of 15); and (3) exteriorization of previous MI patterns (3 of 15). Abnormal Q waves which disappear in the MI course, reappear transiently during an acute ischemic episode. It is emphasized that electrical inertia is not synonymous with irreversible myocardial damage. The significance of transient abnormal Q waves (TAQW) observed during acute coronary insufficiency was studied in 15 patients with atherosclerotic heart disease. TAQW occurred during anginal chest pain (10 of 15), cardiogenic shock (3 of 15) and paroxysmal dyspnea (2 of 15). The anterior myocardial wall was more frequently involved (13 of 15) than the diaphragmatic wall (2 of 15). Serum enzyme levels were normal or slightly increased in 11 of 15. TAQW disappeared in four hours to nine days (mean three days). Three patients died and an autopsy was performed on two of them. It is concluded that cases with TAQW include: (1) acute episodes of myocardial ischemia, without myocardial infarction (MI) (8 of 15); (2) MI with early electrical recovery due to predominant ischemia (4 of 15); and (3) exteriorization of previous MI patterns (3 of 15). Abnormal Q waves which disappear in the MI course, reappear transiently during an acute ischemic episode. It is emphasized that electrical inertia is not synonymous with irreversible myocardial damage.

Vector-Electrocardiographic Exercise Test in Ischemic Heart Disease

Exercise tolerance was measured in 59 subjects with functional class 2, 3, and 3-4 ischemic heart disease with a standardized treadmill exercise, the end point of which was the appearance of an ischemic ST segment, an ischemic T loop, angina, or disabling dyspnea or fatigue. Forty-seven (80%) exhibited an ischemic T loop, but only 35 (60%) exhibited an ischemic ST segment during or after exercise. Twelve of the 59 (20%), therefore, exhibited an ischemic T loop unassociated with an ischemic ST segment. Results were reproducible despite the many variables that influence the course of ischemic heart disease. These results indicate that the duration of this exercise to the appearance of electrocardiographic or vectorcardiographic changes of ischemia represents a practical and objective measure of exercise tolerance in ischemic heart disease.