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Johann Wolfgang von Goethe (1749-1832) underwent a heart attack on March 20th 1832 after suffering from a febrile infection of the airways. Two days later he died under the signs of heart failure. A detailed report is given from his physician Dr. Carl Vogel. Extracts of this document are presented and commented. The last words of Goethe remain unclear.
As recently as five years ago, doctors thought they had a pretty clear picture of what causes a heart attack. They saw it as a plumbing problem: too much fat in the diet builds up in the blood vessels that feed the heart, creating stoppages that starve the heart of oxygen. It was an elegant model and one that patients could understand. But it's not that simple. Cholesterol, it turns out, is just the starting point of a cascade of interlocking events. Underlying the new research presented at the American Heart Association meeting last week was a clear message: this isn't your father's heart disease anymore.
BACKGROUND: In the United States, 2.5 million women have heart failure, yet little is known about their quality of life. Because most studies included small samples of women, the results are not generalizable. OBJECTIVE: To compare the quality of life of women with heart failure with that of a normative group and with that of women with other chronic conditions. METHODS: Descriptive techniques were applied to baseline data collected in the Studies of Left Ventricular Dysfunction trials to characterize quality of life in women with heart failure (n = 691). Global quality of life and the quality-of-life dimensions of physical function, emotional distress, social health, and general health were measured by using the Ladder of Life, items from the Profile of Mood States Inventory, the Functional Status Questionnaire, the Beta Blocker Heart Attack Trial instrument, and an item from the RAND Medical Outcomes Study instrument. RESULTS: Compared with the normative group of women, women with heart failure had significantly lower global quality of life; worse vigor, intermediate activities of daily living, social activity, and general health ratings; and higher ratings for anxiety and depression. Fewer than half of the women with heartfailure felt that they were healthy enough to perform normal activities. CONCLUSIONS: Women with heart failure have worse quality of life than do normative populations and patients with other chronic diseases such as hypertension, Parkinson disease, and cancer.
The incidence of myocardial infarction and the return to work for survivors were studied among the employees of an English car assembly plant by analysing 12 811 medical records of persons employed during the seven years between January 1966 and December 1972. The standardized morbidity ratio of myocardial infarction found in this study calculated on the basis of incidence rates reported by Kinlen )1973) for the Oxford community in which the factory was situated was 90. The standardized morbidity ratio from production line workers only was 66 and that for the monthly paid staff 272. Of the production line workers who survived the attack 22 (90%) returned to their previous jobs without undue difficulty and with two exceptions within four months of the onset of their illness; there was no relation between length of absence and age at the time of attack. These findings suggest that workers in mass production jobs such as car assembly are not special risk from myocardial infarction, and most of those who survive a heart attack are able to return to their former work. Taken with Kinlen's (1973) study and that of Armstrong et al. (1972) in Edinburgh, they also bear out mortality data by indicating that in Oxfordshire the incidence of coronary heart disease is lower than the British average.
Relatively few studies have examined the clinical effectiveness of cholesterol-lowering drugs in women as compared with men. Most clinical trials do indicate that cholesterol lowering reduces clinical events equally effectively in both genders. However, high-density lipoprotein cholesterol and triglyceride levels may have more prognostic significance in women. The recent finding of a higher risk of death in younger women as compared with younger men who sustain a heart attack, combined with the high proportion of morbidity and mortality due to CHD in older women, emphasizes the need for a better understanding of heart disease in women. This review explores the similarities and differences between women and men regarding the management of dyslipidemia.
The ultimate aim in treating hypertension and hyperlipidemia is to reduce cardiovascular mortality and morbidity, especially strokes and coronary events, for example, fatal and nonfatal myocardial infarction and sudden death. Extensive intervention studies in moderate-to-severe hypertension have revealed the significance of antihypertensive therapy in reducing total cardiovascular mortality and morbidity, particularly from cerebrovascular causes. However, the reduction of coronary events has not been equally successful. The situation in mild-to-moderate hypertension is even more disappointing: recent studies, such as the Medical Research Council hypertension trial, the international Prospective Primary Prevention Study in Hypertension, and the Heart Attack Primary Prevention in Hypertensives trial could not demonstrate any benefit from antihypertensive treatment with beta-blockers or diuretics in the prevention of coronary heart disease. The reasons for these negative results are not obvious. However, metabolic side effects associated with certain antihypertensive drugs, which counteract the beneficial effects of blood pressure reduction, are one topic of discussion. For the genesis of atherosclerosis of the coronary vasculature, hyperlipoproteinemia appears to be of greater importance than hypertension and has to be treated simultaneously. Two extensive intervention studies, the Lipid Research Clinics coronary primary prevention trial and the Helsinki Heart Study, showed a significant reduction of coronary events with lipid-lowering treatments with cholestyramine and gemfibrozil, respectively. These findings are in agreement with the results of a recent secondary prevention study, which showed a regression of atherosclerosis in coronary arteries and aortocoronary bypass grafts. Moreover, antihypertensive treatment aimed at a reduction in coronary heart disease has to focus on serum lipids, especially in mild hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiovascular disease (CVD) remains a global economic burden even in the 21st century with 85% of deaths resulting from heart attacks. Despite efforts in reducing the risk factors, and enhancing pharmacotherapeutic strategies, challenges persist in early identification of disease progression and functional recovery of damaged hearts. Targeting mitochondrial dysfunction, a key player in the pathogenesis of CVD has been less successful due to its role in other coexisting diseases. Additionally, it is the only organelle with an agathokakological function that is a remedy and a poison for the cell. In this review, we describe the origins of cardiac mitochondria and the role of heteroplasmy and mitochondrial subpopulations namely the interfibrillar, subsarcolemmal, perinuclear, and intranuclear mitochondria in maintaining cardiac function and in disease-associated remodeling. The cumulative evidence of mitochondrial retrograde communication with the nucleus is addressed, highlighting the need to study the genotype-phenotype relationships of specific organelle functions with CVD by using approaches like genome-wide association study (GWAS). Finally, we discuss the practicality of computational methods combined with single-cell sequencing technologies to address the challenges of genetic screening in the identification of heteroplasmy and contributory genes towards CVD.
It has long been held as scientific fact that soon after birth, cardiomyocytes cease dividing, thus explaining the limited restoration of cardiac function after a heart attack. Recent demonstrations of cardiac myocyte differentiation observed in vitro or after in vivo transplantation of adult stem cells from blood, fat, skeletal muscle, or heart have challenged this view. Analysis of these studies has been complicated by the large disparity in the magnitude of effects seen by different groups and obscured by the recently appreciated process of in vivo stem-cell fusion. We now show a novel population of nonsatellite cells in adult murine skeletal muscle that progress under standard primary cell-culture conditions to autonomously beating cardiomyocytes. Their differentiation into beating cardiomyocytes is characterized here by video microscopy, confocal-detected calcium transients, electron microscopy, immunofluorescent cardiac-specific markers, and single-cell patch recordings of cardiac action potentials. Within 2 d after tail-vein injection of these marked cells into a mouse model of acute infarction, the marked cells are visible in the heart. By 6 d they begin to differentiate without fusing to recipient cardiac cells. Three months later, the tagged cells are visible as striated heart muscle restricted to the region of the cardiac infarct.
This exploratory study examined the role of family interaction in structuring and maintaining high-risk behaviors in difficult-to-manage patients with heart disease and the use of time-limited, social systems-oriented therapy to modify such behaviors. The study was based on the assumption that "difficult to manage" patients with heart disease, ie, those who failed to modify their high-risk behavior patterns following a cardiac event--and their families, in their attempts to deal with the threat of heart attack, would interact with one another in a manner which would maintain, however unintentionally, the patient's high-risk behavior pattern. Nine such "difficult heart families" were referred to the project. In each case the patient's wife was seen individually for a maximum of five clinical interviews for the purpose of modifying her method of dealing with, and presumably maintaining, her husband's high-risk behaviors. Contact with the patient with heart disease was minimal and used for information-gathering only. In each case, when the wife made the prescribed changes in dealing with her husband, a desirable change in one or more of his high-risk behaviors followed.
Aim of the study was to estimate, the relationship between survival, smoking habits, and the results of medical examinations in inland and coastal regions of Croatia. Age and sex stratified sample of general population (1,571 men and 1,793 women, 37-56 years old in 1972; followed in 1982: N = 1,090 men; 1,325 women and/or 1972-1999 controlling vital status). Relative risks and 95% confidence limits were estimated using Cox regression in the model with time dependent covariates, separately by sex. In all regions, the proportion of male smokers decreased between 1972 and 1982. The proportion of female smokers increased, differently in urban and rural regions. During the follow-up between 1972 and 1999, 568 deaths were recorded among men and 382 among women. In men, in addition to age, significant hazards of death were the number of smoked cigarettes per day, body mass index, sedative intake, vital lung capacity (FVC), 100FEV1/VC, systolic blood pressure, electrocardiogram, history of heart attack, and region. In women, in addition to age, significant predictors were the number of smoked cigarettes per day, systolic blood pressure, electrocardiogram, history of heart disease (excluding coronary diseases), and region. Survival relative risk increased with each additional smoked pack of cigarettes by 2.4% in women and 1.3% in men. Regional differences vs. smoking habit were observed. These data emphasize the need for prevention of smoking.
The EMS, ED, neurology, radiology, nursing, laboratory, and pharmacy departments are integral parts of the stroke team system. These are the key departments responsible for the support of the stroke team, or nucleus, which emanates from the departments of neurology and emergency medicine in the author's medical center. In the same way that cardiac victims are treated for "heart attack," so stroke victims should be treated for "brain attack." The emphasis on public awareness to community outreach and senior citizens groups through the aid of the public affairs department of the institution, the American Heart Association, and the National Stroke Association (NSA) has been a tremendous lift in this, the decade of the brain. The Public Broadcasting System and other television channels have helped enormously in publicizing stroke signs and symptoms, new treatment of stroke, and concurrent risk factors. New clinical research for thrombolytics and neuro-protective agents are now in progress to determine the best treatment for the damaged brain. The emphasis is changing: Time is brain. We hope to change the expenditure attributable to rehabilitation and managed care after stroke to the more hopeful prospects of prevention, early treatment, and fast recovery. We can then see that our friends and family members, as victims of stroke, may proceed to independence rather than long-term care facilities or nursing homes. This will be possible only if hospitals and medical centers nationwide adequately gear themselves for the treatment of ischemic stroke through the creation of a core stroke team, finely-honed interdepartmental cooperation, and the development of an efficient ED team that is fully immersed in the ethics and protocol of "brain attack."
A candid and detailed description of the author's heart attack and its aftermath with advice to his colleagues on how to become more proactive in identifying and dealing with the risk factors associated with coronary heart disease.
Improvements in current heart monitoring techniques could reduce the number of heart attacks and resulting deaths. The potential for using time intervals measured between waveforms of the electrocardiogram (ECG), phonocardiogram (PCG), and peripheral blood flow pulse (PP) for heart monitoring was studied. The waveform locations identified in the simultaneously recorded signals included the R- and T-wave peaks of the ECG, the first (S1) and second (S2) sounds of the PCG, and the systolic peak of the PP. The signals were found to be highly consistent from one cardiac cycle to the next. Further, the time intervals measured between the different signals were stable with time. Strong relationships were found between the intervals R to T and R to S2 and the R to R interval. In contrast, R to PP and R to S1 correlated poorly with the R to R but strongly with each other. Additional differences between the measured intervals were revealed by studying changes due to exercise and different body positions. The relationships between the measured intervals were found to be independent of PCG recording location. This study demonstrates the feasibility and potential of using the electrical-contractile indices of heart function for monitoring heart patients. Design of a computer-based monitor using the techniques specified in this study is discussed along with relative strengths and weaknesses of such a system.
Although platelet characteristics have an important influence on ischaemic heart disease, the nature of the association of platelet size and platelet count with death and reinfarction after an index heart attack is unknown. Mean platelet volume (MPV), a determinant of platelet reactivity, was measured in 1716 men six months after myocardial infarction (MI). Deaths and recurrent ischaemic heart disease events were then assessed at two years. MPV was greater in 126 men who had a further ischaemic event (fatal or non-fatal) than in the 1590 men who had no further MI (p less than 0.001). In addition, the MPV was larger in men who died than in those who did not (p less than 0.001). There was no difference in platelet count between these groups. When analysed by quartiles, consistent trends of increasing age-adjusted relative odds of death and recurrent ischaemic events were noted for MPV. MPV did not correlate with known ischaemic heart disease risk factors such as blood pressure, blood lipids, fibrinogen, white cell count, or plasma viscosity. We believe that MPV is a further independent risk factor for recurrent MI.
Care provided by specialist nurses has been shown to improve outcomes for patients with chronic heart failure (CHF), significantly reducing the number of unplanned readmissions, length of hospital stay, hospital costs, and mortality. Most patients develop CHF as a result of coronary artery disease. Once cardiac damage has occurred, the risk of developing heart failure can be reduced by providing appropriate treatment at appropriate dosages. While cardiac rehabilitation clinics provide an opportunity to check drug usage, their prime focus is on optimising patients' physical well being following a heart attack. In addition, evidence suggests that general practitioners are frequently reluctant to initiate appropriate treatments and to up-titrate drug dosages even for patients with diagnosed heart failure. Therefore, to ensure that these patients are not left on starting doses of medications many hospitals are now setting up nurse led post-myocardial infarction (MI) clinics. The Omada programme is a secondary care based, nurse led model of care set up in 1999 to improve the management of CHF by providing appropriate patient education within a nurse led clinic setting, optimising evidence based medication and fostering partnership between health professionals in both primary and secondary care. The model of care is highly applicable to the post-MI setting, where it can ensure that patients receive better care at an earlier stage.
Heart attacks frequently occur in normolipidemic subjects with low concentration of high density lipoproteins (</=35 mg/dL). A low-fat diet is generally recommended to patients with coronary heart disease. A low-fat diet decreases both low density (LDL) and high density lipoproteins (HDL). We have shown that on an Average American Diet, subjects with different HDL-cholesterol (HDL-C) levels have different HDL subpopulation profiles. In low HDL-C subjects (</=35 mg/dL), the apoA-I-only subpopulation alpha(1) is significantly decreased compared to individuals with normal HDL-C levels (>35 mg/dL). We hypothesized that as subjects with low HDL-C already have low HDL concentrations, the major decrease of HDL-C will occur in subjects with normal HDL-C when a low-fat diet is consumed. Normolipidemic male subjects consumed three diets differing in total fat and saturated fat composition (AAD: 37%, Step-1: 28%, Step-2: 24% total fat) for 6 weeks in a three-period double-blind randomized crossover design. Plasma lipids and apolipoproteins were determined and changes in distribution of HDL subpopulations were evaluated. As a result of a low-fat diet, low HDL-C individuals slightly decreased their HDL-C, but substantially decreased their LDL-C resulting in a significant improvement in the LDL-C/HDL-C ratio. However, subjects with normal HDL-C levels decreased both their LDL-C and HDL-C resulting in an unchanged LDL-C/HDL-C ratio. We also observed significant differences in response to low-fat diets in HDL-C and alpha(1) concentrations between low and normal HDL-C subjects. In the normal HDL-C group, consumption of a low-fat diet also resulted in redistribution of apoA-I-containing HDL subpopulations, indicated by a decrease in the large apoA-I-only alpha(1) subpopulation. These data demonstrate that male subjects with low HDL-C respond to a low-fat diet differently than individuals with normal HDL-C.
We developed a Java applet that calculates four different estimates of a person's 10-year risk for heart attack: (1) Estimate based on Framingham equation (2) Framingham equation estimate modified by C-reactive protein (CRP) level (3) Framingham estimate modified by family history of heart disease in parents or siblings (4) Framingham estimate modified by both CRP and family heart disease history. This web-based, family-oriented cardiac risk estimator uniquely considers family history and CRP while estimating risk.
Rupture of the plaque surface, often with thrombosis superimposed, occurs frequently during the evolution of coronary atherosclerotic lesions. It is probably the most important mechanism underlying the sudden, rapid plaque progression responsible for acute coronary syndromes. The risk of plaque rupture depends on plaque type (composition) rather than plaque size (volume), because only plaques rich in soft extracellular lipids are vulnerable (rupture-prone). Most ruptures are tiny, occurring at the periphery of the fibrous cap that covers the lipid-rich core--points where the cap is usually thinnest and most heavily infiltrated by macrophage foam cells. Compared with intact caps, ruptured ones usually have less tensile strength and are more extensible, containing less collagen and glycosaminoglycans, more extracellular lipid, fewer smooth muscle cells, and more macrophages. Progressive extracellular lipid accumulation (lipid core formation) and cap weakening (macrophage related?) predispose the plaque to rupture and determine the actual vulnerability, which may change with time. Luckily, the plaque components responsible for vulnerability (soft lipid and probably macrophages) are apparently most likely to regress with treatment. The dynamic interplay between the actual plaque vulnerability and external stresses ("triggers") probably determines the particular moment and point of rupture, if this occurs. Vulnerability probably plays a more important role in rupture than triggers, because exercise stress testing of patients with advanced coronary artery disease rarely triggers a rupture/thrombus-related acute heart attack. A prerequisite is the presence of a vulnerable plaque.