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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Electrocardiographic abnormalities have been known to occur in the context of neurologic disease for a long time. These changes fall into 2 categories: arrhythmias and repolarization abnormalities. However, until relatively recently these changes were believed to represent purely electrophysiologic alterations and not real heart disease. It is now clear that some patients with neurogenic electrocardiographic changes show cardiac enzyme release and myofibrillar degeneration at autopsy. There are 4 major methods for producing myofibrillar degeneration (i.e., contraction band necrosis or coagulative myocytolysis): catecholamine infusion, stress-steroid, nervous system stimulation and reperfusion. The common thread connecting these 4 methods is the opening of receptor-operated calcium channels, resulting in intense contraction of cardiac muscle. Thus, neurogenic influence over cardiac function may represent a continuum. In the mild reversible circumstance, only the electrocardiographic change will be seen, whereas in the severe, irreversible situation, myofibrillar degeneration will ensue with release of cardiac enzymes. Cardiac cell death may be caused by oxygen free radicals produced by metabolism of catecholamines or reperfusion or both, after variable periods of ischemia. This concept represents a unifying hypothesis, tying together the clinical, physiologic, biochemical and pathologic findings in neurogenic heart disease.
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PMID:Neurogenic heart disease: a unifying hypothesis. 332 64

Surgical risk factors of abdominal aortic disease. Between January 1, 1982 and October 1986, 327 surgical repairs were performed on abdominal aortic obstructive diseases and aneurysms at the St. Luc University Hospital. 150 pre-, per- and postoperative data were collected retrospectively for each patient. Ninety-one per cent of patients were smokers, 57.5 per cent had heart disease, 43 per cent arterial hypertension, 51 per cent peripheral vascular disease and 28 percent had obstructive lung disease. Concerning cardiac morbidity, the post-operative infarction rate was 4.4 per cent in patients who had previously suffered from an infarction, and 1.9 per cent in patients with no previous infarction. Post-operative angina-ischemia rate were respectively 23 and 4.7 per cent. Two hundred and thirty two elective operations resulted in 6 deaths (2.6 per cent) while 95 emergency operations resulted in 34 deaths (35.8 per cent). The causes of the death and the post-operative complications are detailed. The decrease of the morbidity and the mortality rates inherent to this pathology depends on an early diagnosis and surgical treatment by a team, knowledgeable of this pathology, who are able to prevent and correctly treat the complications, especially those affecting the cardiovascular system.
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PMID:[Risk factors in surgery of the abdominal aorta]. 338 30

Between 1972 and 1975, 1832 middle-aged men (40 to 59 years), apparently healthy with no subjective complaints related to heart disease, underwent extensive noninvasive cardiovascular examinations. Additionally, 50 asymptomatic men with an ischemic reaction in the ECG who were subsequently found to have angiographically-documented coronary artery disease, together with the remainder of the cohort, had regular follow-up examinations in yearly intervals. The total observation period ranged up to 14.5 years. In the group with silent ischemia, at 7.5 years, only 17 of the 50 patients had no evidence of progression and the incidence of cardiac events increased continuously thereafter such that at 13.5 years, only six of the 50 had remained stable. At this time, twelve had died (three within the first 7.5 years) and 13 had undergone bypass surgery. The rate of cardiac events in the group with silent ischemia was four to five times higher than that in those with no manifest disease. The study shows that documentation of myocardial ischemia in asymptomatic patients is indicative of the presence of coronary artery disease and is associated commonly with progression of the disease in spite of the absence of angina pectoris.
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PMID:Prognostic importance of silent ischemia during long-term follow-up of patients with coronary artery disease. A short review based on own experience and current literature. 342 43

Many patients with hypertrophic cardiomyopathy (HCM) have signs and symptoms or metabolic and hemodynamic evidence of myocardial ischemia and dysfunction in the absence of extramural coronary atherosclerosis. To investigate the possibility that a form of "small vessel disease" could account for these findings, a histologic analysis of left ventricular myocardium obtained at necropsy was carried out in 48 patients with hypertophic cardiomyopathy and in 68 controls with either normal hearts or acquired heart disease. In HCM, abnormal intramural coronary arteries (IMCA) were characterized by thickening of the vessel wall and an apparent decrease in luminal size (external arterial diameter less than 1500 micron; average 300 micron). The wall thickening was due to proliferation of medial and/or intimal components, particularly smooth muscle cells and collagen. Of the 48 patients with HCM,40 (83%) had abnormal IMCAs located in the ventricular septum (33 patients), anterior left ventricular free wall (20 patients) or posterior free wall (nine patients); an average of 3.0 +/- 0.7 IMCA were identified per tissue section. Altered IMCAs were also significantly more common in tissue sections having considerable myocardial fibrosis (31 out of 42, 74%) than in those with no or mild fibrosis (31 or 102, 30%; p less than 0.001). Abnormal IMCA wera also identified in 3 out of 8 infants who died of HCM before 1 year of age. In contrast, only rare altered IMCA were identified in six (9%) of the 69 control patients, and those arteries showed only mild thickening of the wall and minimal luminal narrowing (abnormal IMCA per section: 0.1 +/- 0.05: p less than 0.001). Moreover, of those patients who did show abnormal IMCA, such vessels were about twenty times more frequent in patients with HCM (0.9 +/- 0.2/cm2 myocardium) than in controls (0.04 +/- 0.02/cm2 myocardium). Hence, abnormal IMCA with markedly thickened walls and narrowed lumens are present in increased numbers in most patients with HCM at necropsy, and may represent a congenital component of the underlying cardiomyopathic process. Although the clinical significance of "small vessel coronary artery disease" in HCM is unclear, the occurrence of structurally altered IMCA within or adjacent to areas of substantial myocardial fibrosis suggests a causal role for these arteries in producing ischemia.
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PMID:Morphologic evidence for "small vessel disease" in patients with hypertrophic cardiomyopathy. 343 79

In addition to radionuclide ventriculography and thallium scintigraphy, already well established in nuclear medicine, assessment of myocardial metabolism is also of interest for diagnosis and follow-up observations in heart disease. Under aerobic conditions and in the fasting state, the heart muscle primarily oxidizes fatty acids; during ischemia, in contrast, there is slowing of fatty acid turnover and increased anaerobic glycolysis. With 11C-palmitic acid, in humans, reduced fatty acid uptake has been documented in infarcted myocardial regions. The analysis of 11C-palmitic acid in dogs showed a three-phased elimination curve in normal myocardium. In ischemic myocardium, there was diminished utilization of free fatty acids and the glucose utilization was concomitantly increased. After insulin-glucose infusion, as well, there was increased glucose utilization and a reduction in fatty acid utilization. Studies with 11C-palmitic acid require the equipment for positron emission tomography (PET); because of the short half-life of 20.3 minutes, the nuclide must be generated by a cyclotron in the immediate vicinity. In the search for well-suited isotopes for use in planar scintigraphy employing a gamma camera, the uptake and elimination of a variety of isotopically-marked fatty acids were measured and compared with the characteristics of 14C-palmitic acid. For 17-123I-heptadecanic acid (IHA) the elimination curve was similar to that of 14C-palmitate: disadvantage, however, was the relatively high percentage of water soluble marked catabolites which required dual parameter analysis by means of 99-m-technetium pertechnetate or 123I sodium iodide to quantify the amount of myocardial fatty acid utilization through subtraction of the externally measured water soluble catabolite from the externally measured total activity. In studies with the gamma camera in fasting patients in whom 2 to 3 mCi IHA was injected intravenously after symptom limited bicycle ergometry, in healthy subjects the elimination halftime for the first rapid phase was 24.4 +/- 4.7 minutes. Patients with angiographically-documented coronary artery disease, in the afflicted myocardial segments, had diminished fatty acid uptake and prolonged elimination halftime as compared with normally perfused segments. In patients with dilated cardiomyopathy there was an inhomogeneous distribution of activity in the myocardium and, in contrast to coronary artery disease, a discordance between local fatty acid uptake and turnover rate. After chronic and acute alcohol consumption there were comparable findings which were shown to be reversible after several weeks of abstinence.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Planar scintigraphy versus PET in measuring fatty acid metabolism of the heart]. 349 62

Pathologic studies of the visceral smooth musculature in humans are scant despite the relatively frequent occurrence of alterations in these muscles in autopsy material. We investigated the different types of lesions of this musculature observed in various conditions associated with ischemia--acute tubular necrosis, congenital heart disease (low output syndrome due to open heart surgery), and necrotizing enterocolitis in premature babies. Control cases included normal rat tissue undergoing autolysis and rigor mortis and bowel resected from patients with ulcerative colitis and Hirschsprung's disease. Four histologically distinct lesions were present on hematoxylin--eosin staining in the ischemic group: contraction bands, wavy fibers, thick waves, and coagulation necrosis. These lesions were absent in the control groups. We conclude that myofibrillar degeneration and necrosis of the visceral musculature are common in disorders associated with visceral ischemia. These changes are not artifacts produced by autolysis, rigor mortis, or technical handling, nor are they induced by nonischemic inflammatory conditions. Catecholamines may play a role in their genesis.
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PMID:Myofibrillar degeneration and necrosis of the visceral smooth musculature: an ischemic visceral myopathy. 361 Jan 32

Nine hundred twelve patients received continuous epidural analgesia administered through an indwelling plastic catheter while undergoing vascular reconstruction of a lower extremity. During a portion of the operative event, the patients were totally, transiently anticoagulated with heparin. None of the patients had an untoward neurologic event that could be attributed to an epidural hematoma. Our results and those of others show that this form of regional analgesia is safe and far outweighs theoretic contraindications when anticoagulation with heparin is planned as a part of the operative event. In the patients with impaired pulmonary ventilation or a cardiac disorder, this method of analgesia offers many advantages over a general anesthetic, such as obviating aspiration pneumonitis and averting prolonged support in the recovery period after completion of the surgical procedure. The regional vasodilation ensuing from the epidural blockade is an additional advantage in patients undergoing vascular reconstruction for lower extremity ischemia.
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PMID:Continuous epidural analgesia in the heparinized vascular surgical patient: a retrospective review of 912 patients. 361 64

The authors report a case of necrotizing enterocolitis which appeared in the first hours of life of a full-term neonate without signs of sepsis. This neonate presented with a severe hypoplasia of the horizontal aorta and very tight coarctation responsible for hepatic, renal and mesenteric ischemia. Reports of enterocolitis as a complication of congenital heart disease are rare and related most often to hypoplastic left heart than to coarctation of the aorta.
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PMID:[A rare cause of neonatal ulcero-necrotizing enterocolitis: aortic coarctation syndrome]. 361 70

Myocardial perfusion scintigraphy with 201-TL was performed in a group of subjects affected by exercise-induced, rate-dependent left bundle branch block (LBBB). The aim of the study was: to define the significance of the exercise-induced conduction abnormality: "primitive" or "ischemic". 14 patients, aging 28-58 years (x = 42), 8 with chest pain (4 typical angina, 4 atypical angina) and 6 without any symptoms were studied. None had history of prior myocardial infarction or clinical and echocardiographic signs of heart disease. LBBB appeared at a heart rate ranging from 70 to 160 beats/min. 6 patients showed repolarization abnormalities (ST changes, deep and negative T wave) suggestive for ischemia, during successive QRS normalization. 201-TL-uptake was normal in 5 subjects; in the remaining 9 ones reversible TL defects were demonstrated in the septum (6), in the septum and apex (2), in the septum and inferior-apical wall (1). No patients had irreversible impaired perfusion. All the patients had normal coronary angiography, with negative ergonovine test for coronary artery spasm. In conclusion, in the majority of our subjects (64%) with exercise-induced LBBB, a reversible TL-uptake defect, usually located in the septum without diagnostic value of obstructive CAD, has been observed. Further studies will establish if the TL-defect is only an "apparent phenomenon" due to contraction abnormality secondary to LBBB, or, on the contrary, an expression of myocardial ischemia with normal coronary vessels as a consequence of the LBBB.
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PMID:[Study of myocardial perfusion by means of scintigraphy with thallium-210 in left bundle branch block induced by exertion]. 366 78

When electrodes are placed at the surface of the thorax, high-amplification electrocardiography (HA-ECG) combined with signal summation as a function of time provides a non-invasive method for detecting electric potentials occurring after the QRS complex of the clinical electrocardiogram. These potentials are called late, and can probably be likened to the "divided" or "fragmented" potentials recorded directly on the heart or in its ventricles near zones of ischemia, infarction or aneurysm. The prevalence of late potentials of ventricular activation (LPVA) and their association with the occurrence of ventricular arrhythmias seems well established, notably in the presence of ventricular aneurysm and anamnesis of severe ventricular arrhythmia. Some studies have shown that detection of LPVAs is of value in identifying heart patients at risk of ventricular arrhythmia or sudden death. Heart disease aside, the presence of LPVAs has been demonstrated in arrhythmogenic right ventricular dysplasia and reported in Fallot's tetralogy after complete correction. A standardization of recordings and a more precise definition of LPVAs are necessary before HA-ECG can become a routine clinical method. Further, the possibility of "beat by beat" recordings with "spatial" summation will allow detection of LPVAs which vary with time and in nature and hence provide a better understanding of the genesis of ventricular arrhythmias.
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PMID:[Late potentials and ventricular arrhythmia]. 374 Jul 75


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