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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In patients with coronary artery disease, radionuclide investigations have documented a high incidence of mental stress-induced myocardial ischemia in the absence of significant electrocardiographic changes and/or angina. To investigate the causes of the low electrocardiographic sensitivity, we recorded body surface maps during mental arithmetic in 22 normal volunteers and 37 postinfarction patients with residual exercise ischemia. Myocardial perfusion was studied with thallium-201 or technetium-99 (SESTAMIBI) planar scans. In 14 patients, body surface maps were also recorded during atrial pacing at the heart rate values achieved during mental stress. While taking the body surface maps, the area from J point to 80 msec after this point (ST-80) was analyzed by integral maps, difference maps, and departure maps (the difference between each patient's difference map and the mean difference map for normal subjects). The body surface mapping criteria for ischemia were a new negative area on the integral maps, a negative potential of more than 2 SD from mean normal values on the difference maps, and a negative departure index of more than 2. Scintigraphy showed asymptomatic myocardial hypoperfusion in 33 patients. Eight patients had significant ST segment depression. The ST-80 integral and difference maps identified 17 ischemic patients. Twenty-four patients presented abnormal departure maps. One patient presented ST depression and abnormal body surface maps without reversible tracer defect. In 14 of 14 patients, atrial pacing did not reproduce the body surface map abnormalities. The analyses of the other electrocardiographic variables showed that in patients with mental stress-induced perfusion defects, only changes of T apex-T offset (aT-eT) interval in Frank leads and changes of maximum negative potential value of aT-eT integral maps significantly differed from those of normal subjects. Our results confirm the low electrocardiographic sensitivity for detecting mental stress-induced myocardial hypoperfusion in postinfarction patients. ST analysis in the body surface map increases the information content of the electrocardiographic signal. T wave analysis appears to offer fewer diagnostic advantages.
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PMID:Electrocardiographic markers of ischemia during mental stress testing in postinfarction patients. Role of body surface mapping. 182 36

This study was designed to investigate the hemodynamic characteristics of cavernous angiomas of the brain. Five adult patients with a cavernous angioma underwent local cortical blood flow studies and vascular pressure measurements during surgery for the excision of the cavernous angioma. Clinical presentation included headache in four patients, seizures in four patients, and recurring diplopia in one patient. Magnetic resonance imaging demonstrated the cavernous angiomas in all patients and revealed an associated small hematoma in two. Four patients with a cerebral cavernous angioma were operated on in the supine position and the remaining patient, whose lesion involved the brain stem, was operated on in the sitting position. Mean local cortical blood flow (+/- standard error of the mean) in the cerebral cortex adjacent to the lesion was 60.5 +/- 8.3 ml/100 gm/min at a mean PaCO2 of 35.0 +/- 0.6 torr. Mean CO2 reactivity was 1.1 +/- 0.2 ml/100 gm/min/torr. The local cortical blood flow results were similar to established normal control findings. Mean pressure within the lesion in the patients undergoing surgery while supine was 38.2 +/- 0.5 mm Hg; a slight decline in cavernous angioma pressure occurred with a drop in mean systemic arterial blood pressure and PaCO2. Mean pressure in the cavernous angioma in the patient operated on in the sitting position was 7 mm Hg. Jugular compression resulted in a 9-mm Hg rise in cavernous angioma pressure in one supine patient but no change in the patient in the sitting position. Direct microscopic observation revealed slow circulation within the lesions. The hemodynamic features demonstrated in this study indicate that cavernous angiomas are relatively passive vascular anomalies that are unlikely to produce ischemia in adjacent brain. Frank hemorrhage would be expected to be self-limiting because of relatively low driving pressures.
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PMID:Vascular pressures and cortical blood flow in cavernous angioma of the brain. 239 87

1. Isovolumic left ventricular pressure was measured at various coronary arterial pressures in Langendorff-perfused ferret hearts. The concentrations of phosphorus-containing metabolites were measured using 31P nuclear magnetic resonance (NMR). Intracellular free calcium concentration ([Ca2+]i), was measured with 19F NMR in a group of hearts that were loaded with the calcium indicator 5F-BAPTA. 2. Developed pressure increased when coronary arterial pressure was raised from the control value of 80 to 100-160 mmHg and decreased when coronary pressure was lowered to 40-70 mmHg. The changes were reversible. 3. Coronary flow varied directly with coronary pressure over the entire range from 40 to 160 mmHg. 4. The concentrations of phosphorus-containing metabolites and the efflux of lactate from the heart remained unchanged at coronary pressures of 60 mmHg or higher. Below 60 mmHg, intracellular pH decreased, while inorganic phosphate concentration and lactate efflux increased. 5. In contrast to the developed pressure during twitch contractions, maximal Ca2+-activated pressure remained constant at coronary pressures of 60-160 mmHg. Only below a coronary pressure of 60 mmHg did maximal Ca2+-activated pressure decline. 6. An increase in coronary pressure produced an increase in developed pressure even in hearts stretched to the peak of the Frank-Starling relation. 7. When coronary pressure was lowered from 80 to 60 mmHg, [Ca2+]i decreased during systole; the opposite effect was apparent when coronary pressure was raised from 80 to 120 mmHg. 8. We conclude that coronary perfusion (pressure or flow) modulates intracellular calcium and, consequently, contractile force. Ischaemia cannot fully explain this phenomenon, nor can changes in sarcomere length.
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PMID:Cellular mechanism of the modulation of contractile function by coronary perfusion pressure in ferret hearts. 260 38

Bioenergetic and hemodynamic consequences of cellular redox manipulations by 0.2-20 mM pyruvate were compared with those due to adrenergic stress (0.7-1.1 microM norepinephrine) using isolated working guinea-pig hearts under the conditions of normoxia, low-flow ischemia, and reperfusion. 5 mM glucose (+ 5 U/l insulin) + 5 mM lactate were the basal energy-yielding substrates. To stabilize left ventricular enddiastolic pressure, ventricular filling pressure was held at 12 cmH2O under all conditions; this preload control minimized Frank-Starling effects on ventricular inotropism. Global low-flow ischemia was induced by reducing aortic pressure to levels (20-10 cmH2O) below the coronary autoregulatory reserve. Reactants of the creatine kinase, including H+ and other key metabolites, were measured by enzymatic, HPLC, and polarographic techniques. In normoxic hearts, norepinephrine stimulations of inotropism, heart rate x pressure product, and oxygen consumption (MVO2) were associated with a fall in the cytosolic phosphorylation potential [( ATP]/[( ADP].[Pi]] as judged by the creatine kinase equilibrium. In contrast, infusion of excess pyruvate (5 mM) markedly increased [ATP]/[( ADP].[Pi]) and ventricular work output, while intracellular phosphate decreased; MVO2 remained constant under the same conditions. During reperfusion following ischemia, pyruvate effected striking and concentration-dependent increases in MVO2, phosphorylation potential, and inotropism. Pyruvate dehydrogenase flux was augmented during reperfusion hyperemia followed by near-complete recoveries of [ATP]/([ADP].[Pi]), contractile force, heart rate x pressure product, and MVO2 in the presence of 5-10 mM pyruvate. Pyruvate also attenuated ischemic adenylate degradation. Omission of glucose from the perfusion medium rendered pyruvate ineffective in postischemic hearts. Similarly, excess lactate (5-15 mM) or acetate (5 mM) failed to reenergize reperfused hearts and severe depressions of MVO2 and inotropism developed despite the presence of glucose. Apparently, subcellular redox manipulations by pyruvate dissociated stimulated mitochondrial respiration and increased inotropism from low cytosolic phosphorylation potentials. This was evidence against the extramitochondrial [ADP].[Pi]/[ATP] ratio being the primary factor in the control of mitochondrial respiration. The mechanism of pyruvate enhancement of inotropism during normoxia and reperfusion is probably multifactorial. Thermodynamic effects on subcellular [NADH]/[NAD+] ratios are coupled with a rise in the cytosolic [ATP]/[( ADP].[Pi]) ratio at constant (normoxia) or increased (reperfusion) MVO2.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Pyruvate-enhanced phosphorylation potential and inotropism in normoxic and postischemic isolated working heart. Near-complete prevention of reperfusion contractile failure. 270 62

Computerized interpretation of the electrocardiogram has now advanced to computerization of the electrocardiograph, resulting in greatly increased versatility, including the capacity for adapting to a variety of lead systems rather than being tethered to the old Einthoven-Wilson-Goldberger (EWG) system. Many varieties of display beyond the 12-lead ECG are also available in software. To date, these new and interesting capabilities have scarcely been exploited. The EASI lead system uses the E, A, and I electrode positions of the Frank lead system, plus an electrode, S, positioned over the upper end of the sternum and, if necessary, ground (anywhere convenient). Its outputs form quasi-xyz signals, x'y'z', that can be approximately transformed into xyz signals by means of a matrix derived from the EASI lead vectors. The result forms a good basis for deriving the 12-lead ECG, using previously published coefficients for the Frank lead system. The match with the conventional ECG can then be improved by statistical means. The results are surprisingly good, and certainly of clinical value. Recent widespread interest in silent ischemia and its detection through Holter monitoring suggests an immediate application which has been rendered practical by the recent introduction of three-channel recorders. The EASI electrode positions give technically satisfactory Holter recordings. Very compact three-channel, multiplexed, radio telemetry equipment is now commercially available and provides another application for the EASI 12-lead ECG.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Deriving the 12-lead electrocardiogram from four (EASI) electrodes. 321 72

While the total ischemic burden on the left ventricle represents the combined effects of both symptomatic and asymptomatic myocardial ischemia, the total vascular burden has many components including an increased systemic peripheral vascular resistance, an increased pulmonary vascular resistance, and an increased coronary vascular resistance. These factors may all influence ventricular function. Hypertension contributes significantly to the vascular burden, especially when combined with left ventricular hypertrophy, which predisposes to ischemia by multiple mechanisms. In patients with hypertension and cardiomegaly, sublingual nifedipine has been shown to increase left ventricular (LV) ejection fraction and the average diastolic filling rate. In the presence of acute myocardial infarction, nifedipine moves the LV function curve onto a better Frank-Starling relationship as pulmonary wedge pressure falls or stays the same and cardiac output rises. However, because of the delicate balance between myocardial perfusion and the benefits of afterload reduction, including improved remodelling, nifedipine should be given only to selected patients. In congestive heart failure, low-dose nifedipine reduces the afterload and has been shown to have beneficial effects in the majority of patients. Two specific adverse outcomes in only two patients have been reported, one with initial hypotension and one given high-dose nifedipine. Combination nifedipine-beta blocker therapy has been shown to be favorable in the treatment of all varieties of angina, hypertension, and hypertrophic cardiomyopathy. Therefore, when administered appropriately, nifedipine reduces the total vascular burden on the heart in a variety of cardiovascular diseases, with consequent improvement in LV function and a diminished threat of potential myocardial ischemia.
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PMID:The total vascular burden, peripheral and coronary: vasodilator effects of nifedipine. 327 10

To determine the essential mechanism of increased systolic wall motion, i.e., hyperkinesis, in a nonischemic region (NIR) during acute ischemia, we simultaneously evaluated global and regional function of the excised, cross-circulated canine left ventricle connected to a volume servo pump before and after coronary occlusion. Regional areas were determined with pairs of orthogonal subendocardial sonomicrometers in the ischemic region (IR) and NIR. After coronary occlusion with left ventricular end-diastolic and stroke volumes kept constant, the amount of systolic area shrinkage (delta A) in NIR increased by 33 +/- 41% (p less than .05), despite a decrease in end-diastolic regional area by 3 +/- 4% (p less than .05). Regional work obtained from the wall tension-regional area (T-A) loop in NIR decreased by 50 +/- 24% due to a similar decrease in afterload despite the presence of hyperkinesis, indicating regional systolic unloading. When left ventricular end-diastolic volume was subsequently increased with a constant stroke volume, delta A in NIR increased at the expense of a further decrease in delta A in IR. The end-systolic T-A relationship in NIR remained unchanged, whereas that in IR markedly shifted rightward, suggesting that the contractile state of NIR was constant. These results indicate that hyperkinesis in NIR during acute ischemia can occur without a utilization of the Frank-Starling mechanism or an enhancement of regional contractile state, and that the essential mechanism of this phenomenon is regional afterload reduction due to an intraventricular mechanical interaction between IR and NIR.
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PMID:Hyperkinesis without the Frank-Starling mechanism in a nonischemic region of acutely ischemic excised canine heart. 333 35

We evaluated left ventricular (LV) regional work from a wall tension-regional area (T-A) loop using sonomicrometers in the excised cross-circulated canine left ventricle connected to a volume servo pump. Regional work assessed from a T-A loop closely agreed with the predicted value calculated from LV stroke work and percent regional area under conditions of the control state, dobutamine infusion, and global ischemia. In addition, globally integrated regional work over the entire ischemic and non-ischemic zones agreed closely with LV stroke work either before or after coronary occlusion. These results indicate that LV regional work can be assessed reliably from the T-A loop in both normal and regionally ischemic hearts. Regional work correlated linearly with end-diastolic regional area, indicating a regional Frank-Starling relation, and the slope of this relationship increased with dobutamine infusion and decreased with global ischemia. The correlation between regional work and LV stroke work was also linear and the regression line was the same during the control state and global ischemia, indicating a constant relationship between the work of a specific wall region and LV stroke work regardless of global changes in contractile state. However, after regional ischemia, this regression line apparently shifted downward because T-A loops in the ischemic region were extremely deformed and regional work markedly decreased. From these results, we conclude that T-A loops are a reliable and useful means of assessing regional contractile performance of the LV.
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PMID:Quantitative evaluation of left ventricular regional work from wall tension-regional area loop in canine heart. 358 3

We clarified that the set of the isotropic component (T) of wall tension and the area (A) of a selected region of the left ventricular wall expresses the regional work with sufficient accuracy. The area surrounded by the locus of the T-A relation in the T-A plane is approximately equal to the real work done by that region. The behavior of the T-A loop was studied in nine anesthetized dogs under various conditions. The regional area and diameter of the left ventricle were measured with ultrasonic crystal pairs. The wall tension was calculated from measured left ventricular pressure and diameter by a generalized Laplace's equation for a thick-walled model. During volume loading, administration of methoxamine, and aortic constriction, the regional work per stroke increased with the increase in end-diastolic regional area, which is considered to be the regional Frank-Starling mechanism. With the development of ischemia, the T-A loop for the ischemic region shifted to the right and the work done by that region decreased. After a certain stage in the development of ischemia, the work done by the ischemic region became negative. When only one of the segmental lengths, rather than the area, is measured, difficulty arises in the physical interpretation of pressure-length or tension-length data in some cases. The T-A loop diagram resolves such difficulty by defining the regional work correctly. We conclude that the T-A loop diagram is a useful tool for analyzing the regional ventricular function.
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PMID:Regional work of the ventricle: wall tension--area relation. 383 Oct 20

We used radionuclide angiography during right atrial pacing to assess left ventricular function in 7 normal subjects and 20 patients with coronary artery disease. A left ventricular function curve relating stroke volume to end-diastolic volume was plotted for each patient. The normal pacing ventricular function curve was a straight line passing through the origin of axes. The pacing ventricular function curve was abnormal in 18 of the 20 patients with coronary artery disease, and three different shaped curves were obtained, reflecting decreased contractile force for the same end-diastolic volume during ischemia. Cardiac output and blood pressure do not change during atrial pacing, thus the Frank-Starling relationship is evaluated by this method during almost experimentally controlled conditions. Relating stroke volume to end-diastolic volume, and not end-diastolic pressure, distinguishes between overall left ventricular systolic function and left ventricular compliance.
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PMID:Radionuclide left ventricular function curve during atrial pacing in normal subjects and in patients with coronary artery disease. 394 44


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