[Cardiac insufficiency due to ischemic heart disease - hypertension, ischemic heart disease and myocardial infarct].
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Heart failure (HF) is a progressively debilitating disorder characterized by frequent hospital admissions and high annual mortality rates. Coronary artery disease (CAD), hypertension, and aging are major risk factors for the development/progression of HF. For years, most of the attention has been focused on HF caused by reduced left ventricular (LV) systolic function, largely attributable to CAD. It is now generally accepted that nearly 50% of elderly patients with HF might have normal or preserved LV systolic function. This condition is commonly referred to as a distinct type of HF caused by LV diastolic dysfunction, and it often accompanies hypertensive heart disease. Isolated diastolic HF is increasingly recognized as the dominant cause of symptoms and hospitalizations from HF in a large proportion of individuals aged 65 and older. However, the clinicians caring for patients with diastolic HF do not fully understand its cause, how it progresses, or how it could be appropriately diagnosed and treated. Because varying degrees of systolic and diastolic dysfunction might coexist in any individual patient, and given the limitation of current diagnostic tools, the overall impact of isolated diastolic HF continues to evolve. Ongoing clinical trials are testing new strategies for treatment of diastolic HF.
Heart function can be investigated non-invasively and without risk for the patient by means of radionuclide ventriculography. Coronary artery disease can be diagnosed with high sensitivity and distinguished from other diseases of the heart with high specificity by typical alterations of heart function as seen in rest and/or exercise scans. The hemodynamic significance of invasively proven stenoses of coronary arteries can de demonstrated and the function and functional capacity of surviving vital myocardium after myocardial infarction can be quantified scintigraphically. The efficacy of medical and surgical therapy can be documented and the course of disease can be followed up.
BACKGROUND: In all 8353 women and 7058 men aged 45-64 took part in the Renfrew/Paisley survey in 1972-1976. They formed a prospective cohort study of a general population in the West of Scotland; an area with high ischaemic heart disease (IHD) mortality rates. The objective of this study was to investigate three indicators of pre-existing IHD and determine how they predicted subsequent IHD mortality in females compared with males. METHODS: Pre-existing IHD was ascertained by the Rose Angina questionnaire, a question on severe chest pain indicating evidence of previous IHD and an electrocardiogram at a screening examination. Mortality information for a 15-year follow-up period was available. RESULTS: Pre-existing IHD was higher at older ages and was less common in women than men. The risks of IHD mortality were doubled for those with a single cardiovascular indicator compared to those without, and were increased to fourfold for those with two or more indicators. Indicators of pre-existing IHD had high specificity and low sensitivity for subsequent IHD mortality in both women and men, and the positive predictive values for women in the oldest age group were similar to those for men in the youngest age group. CONCLUSIONS: Each indicator of pre-existing IHD was a useful predictor of subsequent IHD mortality in both women and men, even though IHD mortality rates were lower in women. The indicators obtained by questionnaire could be implemented in the primary health care setting to identify quickly those at risk who would benefit from further investigation and intervention.
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Halothane was administered at an end-tidal concentration of 1% to 10 patients with stable ischaemic heart disease and clinical and haemodymanic signs of moderate heart failure. Measurements of central haemodynamic variables, coronary sinus blood flow and oxygen, lactate and hypoxanthine balances over the myocardium were done before and at steady state during halothane anaesthesia. Halothane induced marked haemodynamic changes with decreases in mean arterial pressure (-43%), mean pulmonary arteriolar occlusion pressure (-42%), systemic vascular resistance (-31%), cardiac index (-20%) stoke volume index (-31%) and left and right stroke work indices (-62% and -55%, respectively). Heart rate and pulmonary vascular resistance did not change. Coronary sinus blood flow decreased in parallel with perfusion pressure, and myocardial oxygen consumption decreased (-40%), as did myocardial oxygen extraction. Rate pressure product and triple product correlated better with changes in myocardial oxygen consumption in the present subset of patients than in healthy volunteers during halothane anaesthesia. The findings suggest that halothane, through its systemic vasodilatory effect, unloads the failing left ventricle and that this peripheral action predominates over the direct cardiodepressant action of the agent. The combined findings of unchanged coronary vascular resistance, decreased myocardial oxygen extraction and absence of increasing or pathological levels of lactate and hypoxanthine in coronary sinus blood imply a direct dilatory effect of halothane on the coronary vasculature.
Separate weights for heart ventricle walls and interventricular septa were analyzed in 110 hearts with autopsy findings of ischemic heart disease (coronary atherosclerosis, recent or old myocardial infarcts) and with no other cardiac or systemic causes of cardiac enlargement. In hearts with coronary atherosclerosis alone (without old or recent myocardial infarcts) no weight increase was observed in the left ventricle when compared to 29 controls. Patients having infarcts associated with nonstenosing atherosclerosis (less than 50% of the luminal diameter narrowed) of the coronaries had normal heart weights as well. On the contrary, infarcts associated with stenosing coronary sclerosis (narrowing more than 50%) showed significant signs of left ventricular weight increase, which is interpreted as compensatory heart hypertrophy. The greatest degree of hypertrophy was observed in hearts with left ventricular aneurysms.
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The importance of metals in normal and pathologic cardiovascular function has been recognized. Significant derangements in myocardial Ca2+, Mg2+, and Cu2+ have been reported in ischemic heart injury. We studied 3 groups of hearts: 1) fifteen specimens obtained from patients who had no heart disease, 2) nine specimens from patients who had expired from cyanotic congenital heart disease, and 3) ten specimens from patients who had expired from acute rheumatic heart disease with carditis and severe heart failure. None of the patients had undergone cardiac surgery. Left ventricular lateral wall Mg2+, Ca2+, Cu2+, and Zn2+ contents were measured by atomic absorption spectrometry. The results showed a significant decrease in myocardial Mg2- (Group I 177.06 +/- 32.71; Group II 155.66 +/- 14.79; Group III 149.00 +/- 13.29, p less than 0.05 and p less than 0.01, respectively), and Cu2+ contents (Group I 3.22 +/- 0.37; Group II 2.94 +/- 0.22; Group III 2.56 +/- 0.32, p less than 0.02 and p less than 0.001, respectively), and a rise in myocardial Ca2+ content (Group I 36.06 +/- 10.72; Group II 43.22 +/- 7.01; Group III 46.30 +/- 4.85, p = not significant, and p less than 0.01, respectively). The myocardial Zn2+ content did not change significantly (Group I 26.53 +/- 3.99; Group II 26.00 +/- 4.15; Group III 26.40 +/- 3.53). The myocardial Mg2+/Ca2+ ratio was reduced markedly in both groups (Group I 5.328 +/- 1.879; Group II 3.685 +/- 0.735; Group III 3.135 +/- 0.291, p less than 0.001 for both Groups II and III vs Group I). The latter results correlated closely with the myocardial Mg2+/Ca2+ ratios reported in experimental models in peri-infarction zones. Thus, the myocardium of patients who had expired from cyanotic congenital heart disease and acute rheumatic carditis is jeopardized by ischemia, with metal contents similar to the border areas in myocardial infarction.
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We examined retrospectively 186 patients with acute coronary syndrome (ACS) and 163 patients with cardiac insufficiency (CHF) regarding secondary prevention in hospital or externally. Of the Inhospital-patients with ACS 99% had antithrombotic medicaments (AT), 73% betablockers and 73% a statin. CHF-patients had ACEH in 69%. Externally 120 patients with known coronary heart disease (CHD) received in 91% AT, 66% betablocker, 30% statins and 111 CHF-patients in 49% ACEH. Compared to other studies medical therapy ameliorated in CHD and CHF either stationary and ambulatory. The reasons for low prescription of statins may be due to short time since positive results occurred and to the expensive costs in the setting of pressure because of high cost in health system.
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