Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cyclical changes in heart rate and systemic blood pressure that accompany apneic events are predominantly mediated by fluctuations in the activity of the autonomic nervous system. Increased vagal efferent parasympathetic activity is responsible for the cyclical reductions in heart rate during apnea. In contrast, the cyclical elevations in systemic blood pressure are believed to result from recurrent peripheral vasoconstriction mediated by repetitive activation of the sympathetic nervous system. Maximal activation and pressures coincide with apnea termination and brief arousal from sleep. These cyclical elevations in systemic pressure during sleep increase ventricular workload and, thereby, may contribute to the development of ventricular hypertrophy. Systemic hypertension is present during wakefulness in approximately 50% of patients with OSA. Although age and obesity are the predominant risk factors for diurnal hypertension, OSA probably makes an independent contribution in younger obese men. Sinus bradycardia, Mobitz type 1 second-degree heart block, and prolonged sinus arrest have all been documented in association with the apneic events. Increased ventricular ectopy has been observed with oxyhemoglobin desaturations below 60%. Myocardial ischemia, infarction, sudden death, and stroke all demonstrate similar circadian variations in time of onset. Peak frequencies occur between 6 AM and noon, generally within several hours of awakening. Although sleep is associated with decreased frequencies of these adverse cardiovascular events in the general population, evidence exists linking REM sleep to an increased risk of myocardial ischemia. In men who habitually snore, epidemiologic data have detected an increased risk for ischemic heart disease and stroke. Habitual snoring has also been associated with an increased risk of sudden death during sleep. In patients with clinically significant OSA, there is reasonable information indicating excessive mortality in the absence of treatment. This mortality is predominantly cardiovascular and tends to occur during sleep.
 ...
PMID:Hypertension, cardiac arrhythmias, myocardial infarction, and stroke in relation to obstructive sleep apnea. 152 12

To study the effect of apnea and hypoventilation-induced hypoxemia on the heart, we carried out polysomnographic recordings over 4 nights with electrocardiographic tracings in 30 patients with and without coronary heart disease. Evaluations of the data were based on the 2nd and 4th nights. In six subjects, five with coronary heart disease, we found 85 episodes of nocturnal ischemia, mainly during REM sleep (83.5%), high apnea activity, and sustained and progressive hypoxemia. Complex ventricular ectopy was observed in 14/13 patients (nights 2/4) and repetitive ventricular ectopy in 5/3. There was no significant difference in the quality and quantity of ventricular ectopy during wake and sleep states between the CHD group and the control group. In one patient ventricular bigeminy was observed only at a threshold of SaO2 below 60%. Bradyarrhythmia was made evident in four subjects from the CHD group and correlated mainly with apnea activity. We suppose that patients with sleep apnea and CHD are at cardiac risk because coronary heart disease can be aggravated by insufficient arterial oxygen supply due to cumulative phase of apnea and hypoventilation. The reduced hypoxic tolerance of the heart may lead to myocardial ischemia and increased electrical instability.
 ...
PMID:Nocturnal myocardial ischemia and cardiac arrhythmia in patients with sleep apnea with and without coronary heart disease. 192 Dec 30

The aim of the study was the assessment of the sensitivity, specificity and accuracy of some ECG criteria of left ventricular hypertrophy (LVH). Left ventricular mass (LVM) measured on the M-mode echogram of the left ventricle was the reference standard. Ninety-four (94) unselected, consecutive clinical patients (34 women, 60 men, average age 47 years) underwent in the same day, ECG and echocardiogram. Exclusion criteria were the presence of ischemic heart disease, atrial fibrillation and Wolff-Parkinson-White syndrome. The ECG tracings were interpreted independently by 2 investigators following 5 independent criteria of LVH: 1) Sokolow-Lyon voltage criterion (SL); 2) a modified Romhilt-Estes point score (REM); 3) left atrial abnormality (LAA); 4) left ventricular strain; 5) a new voltage criterion RaVL + SV3 corrected by sex and age. The left ventricular M-mode echograms were recorded using a left parasternal approach and were interpreted independently by 2 investigators. LVM was measured using the "Penn convention" and taking the R wave peak as end-diastole. The prevalence of LVH (= LVM 215 g) in the study population was 47%. The following results were achieved (sensitivity, specificity, accuracy): SL: 68.2%, 84%, 76.6%; REM: 63.6%, 90%, 77.7%: LAA: 36.4%, 84%, 61.7%; strain 52.3%, 72%, 62.8%; RaVL + SV3: 54.5%, 82%, 69.1%. Our data suggest: 1) the high sensitivity, specificity and accuracy of Romhilt-Estes point score are confirmed; 2) the sensitivity of Sokolow-Lyon voltage criterion is reevaluated; 3) the most sensitive morphological criterion seems to be the left ventricular strain; 4) a new voltage criterion could be useful.
 ...
PMID:[Validity of some electrocardiographic criteria in left ventricular hypertrophy]. 252 30

This review summarizes briefly the present knowledge on sleep-related factors in ischaemic heart disease. A marked circadian rhythm in the frequency of onset of acute myocardial infarction has been found, but the exact mechanism is not known. The circadian variation is possibly explained by several mechanisms. The best documented is sleep apnoea syndrome, which seems to be a risk factor for ischaemic heart disease and stroke. Stressful REM-sleep seems to be potentially arrhythmogenic in patients with decreased cardiopulmonary function. The role of coronary spasm, increased thrombocyte aggregation and mental stress in sleep disorders is still poorly understood.
 ...
PMID:Cardiovascular stress and sleep. 331 Aug 37

Contributions by 3 major spontaneous oscillatory heart rhythm (HR) components have been analyzed in 20 healthy subjects and 75 ischemic heart disease (IHD) patients during wakefulness and individual sleep stages. Stages of sleep were scored manually based on polygraphic recording of EEG, EOG and EMG throughout the night. HR was fed into the computer continuously for evaluation of the contributions by high- (HFC), medium- (MFC), and low- (LFC) -frequency components to the HR power spectrum. In the healthy subjects, relative contributions by the oscillatory components did not differ during wakefulness, but HFC and LFC prevailed during deep sleep and during REM sleep, respectively. The sleep-mediated changes were related with a more marked decrease in LFC and MFC during deep sleep and an increase during REM sleep as compared with HFC changes. The lower total HR variability in the IHD patients during wakefulness and individual sleep stages was paralleled by a relative increase in LFC whose values were dependent upon the functional state of the IHD patients. The differences in relative contributions by the HR oscillatory components in the IHD patients were related to a more marked decrease in the share of HFC and MFC in the patients as compared with the healthy subjects.
 ...
PMID:Components of the heart rhythm power spectrum in wakefulness and individual sleep stages. 373 90

Portable 24-hour polygraphic monitorings were performed on 109 cases with neurological or cardiovascular disorders, sleep disturbances and metabolic diseases to clarify its usefulness and limitations. Moreover, an evaluation of autonomic nervous activity was done in different stages of sleep in normal young (n = 9), normal middle-aged subjects (n = 8) and patients with ischemic heart disease (n = 7) using power spectral analysis of heart rate. The parameters recorded in this study were electroencepharogram(EEG), electrooculogram, electromyogram of chin muscles, electrocardiogram, respiratory curve, walking pulse and body position. Using polygraphic monitoring, the patients with cardiac arrhythmia showed abnormal EEG in 20% and those with neurological events in 86.7%. The improvement of sleep structure was found after pacemaker implantation in the patients with bradyarrhythmias (75%). Time spans of slow wave sleep and REM sleep of patients with ischemic heart disease decreased significantly from 120.9 +/- 40.6 min to 79.1 +/- 25.3 min, 112.8 +/- 16.5 min to 63.6 +/- 23.6 min, respectively (p < 0.05). RR50, that is number of R -R intervals greater than 50msec compared to the preceding R-R interval, decreased significantly in each stage of sleep in the patients with ischemic heart disease compared to normal subjects (stage 2: 18.3 +/- 6.1/min to 3.8 +/- 3.0/min, p < 0.01; SWS: 7.8 +/- 8.0/min to 3.2 +/- 2.5/min, p < 0.05; REM: 17.9 +/- 6.0/min to 4.4 +/- 4.3/min, p < 0.01). The HF power in all stages of sleep showed a trend of the decrease in the patients with ischemic heart disease. In REM sleep, the LF power in patients with ischemic disease was lower significantly compared to that in normal middle-aged subjects (6.1 +/- 3.2 to 12.1 +/- 4.1, p < 0.05). The L/H ratio also decreased significantly (1.08 +/- 0.30 vs. 2.35 +/- 1.03, p < 0.05). The slope of 1/fx above 0.15Hz in IHD patients was less in stage 2 (-0.404 +/- 0.280 vs. -0.849 +/- 0.183, p < 0.01) and in REM sleep (-0.294 +/- 0.368 vs. -0.665 +/- 0.291, p < 0.05). Above results suggest the involvement of a decrease of sympathetic activity in addition to decrease of parasympathetic activity especially in REM sleep in the patients with ischemic heart disease. In conclusion, polygraphic monitoring is useful for a detection of abnormality of EEG and an evaluation of autonomic activity in cardiovascular disorders.
 ...
PMID:[The usefulness of portable 24-hour polygraphic monitoring--evaluation of autonomic nervous activity of the patients with ischemic heart disease by using heart rate variability during sleep]. 772 82

In normal subjects, the level and variability of blood pressure decrease during non-rapid eye movement (non-REM) sleep. In contrast, sleep apnea is associated with large swings in nocturnal pressure. In this study, we evaluated a computer-derived index of all-night blood pressure variability in normotensive snorers with or without sleep apnea. We also examined this index in snorers receiving medical treatment for coexistent ischemic heart disease. Beat-to-beat blood pressure was recorded with a photoplethysmographic device (Finapres) throughout polysomnography. Subjects were categorized into four groups: those without cardiovascular disease without or with sleep apnea (> or = 15 apnea plus hypopnea per hour of sleep), and those with ischemic heart disease without or with sleep apnea. A frequency distribution histogram of all increases and decreases of blood pressure according to their amplitudes was drawn and the SD of the distribution used as an estimation of variability. Mean systolic and diastolic pressures during the total sleep time were not different among the four groups. In contrast, the SD of the distribution of systolic and diastolic pressure variations that were higher in the apneic than in the nonapneic groups (P < .05) correlated with apnea plus hypopnea (P < .0001) and transient electroencephalographic arousal number per hour of sleep (P < .0001). In both apneic and nonapneic subjects, blood pressure variability as assessed by SD decreased during stages 3 and 4 of non-REM sleep compared with stages 1 and 2 and REM sleep (P < .001). Blood pressure variability was similarly increased in apneic subjects with or without ischemic heart disease. We speculate that in apneic individuals with coexistent ischemic heart disease, pressure variability that is increased despite treatment with beta-blockers or calcium antagonists may be a risk factor for acute coronary events.
 ...
PMID:Short-term variability of blood pressure during sleep in snorers with or without apnea. 895 80