Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myocardial lactate (L) metabolism was tested in 27 stable angina patients during atrial pacing (AP) and in the recovery period (R) from AP-induced angina pectoris. The recovery period was assessed in order to evaluate the changes in the rate of L release and detect possible relationships with the severity of ischaemic damage. The following variables were assessed: coronary sinus blood flow (CSBF), left ventricular end-diastolic pressure (LVEDP), lactate extraction ratio (L%), lactate extraction or release rate (LR) and myocardial oxygen consumption (MVO2) at the onset of AP (AP1), during angina (AP2), and 30 s, 2 and 4 min (R1, R2 and R3) after AP ceased. At Ap2, negative L% and LR values (-39.37 +/- 43.3, -3.2 +/- 2.9) were found, in spite of a rise in CSBF (+86%, P less than 0.001). Furthermore, LVEDP showed its maximal increase in AP2 (+27%, P less than 0.001). Compared to AP2, L% resulted unchanged in R1, while LR showed a mild decrease (from -3.2 +/- 2.9 to +2.06 +/- 2.93). Lactate production was converted to extraction in R3 only. Since lactate production and release are progressively reduced with increasing severity of ischaemic damage, AP2 coronary sinus lactate release should largely arise from the less damaged areas (i.e. the outer myocardial layers) and the contribution of the more damaged areas (i.e. the inner myocardial layers) should be more limited. After AP ceases, the mild ischaemic areas should recover more rapidly than the severely ischaemic areas, where the damage only declines, leading to a temporary increase in lactate production and release.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lactate release during the recovery period of pacing-induced angina in assessment of myocardial ischaemia. 395 25

The different mechanisms of action of beta-blockers and calcium antagonists could result in an additive therapeutic effect in patients with angina pectoris. Twenty-one male patients aged between 41 and 68 years and suffering from chronic stable angina pectoris and coronary artery disease confirmed by angiography took part in a randomized, double-blind study to examine the acute effect of 10 mg of bisoprolol, 20 mg of nifedipine, and a combination of the two drugs on hemodynamics at rest and during exercise [heart rate (HR), systolic blood pressure (SBP), rate-pressure product (RPP), cardiac index (CI), total peripheral resistance (TPR), and pulmonary capillary wedge pressure (PCP)], the behavior of the ST segment (ST), and exercise tolerance until occurrence of an ST-segment depression of 0.1 mV (W-ST01) and until onset of anginal pain (W-AP1). Following a baseline exercise test, 11 patients were given 10 mg of bisoprolol orally, whereas 10 patients received placebo. Two hours later, a second exercise test was carried out. All patients in both groups then received 20 mg of N orally. A third exercise test was performed 2 h later. On exercise, bisoprolol resulted in significant changes in HR (-16%), RPP (-22%), and CI (-16%), as well as in TPR (+ 13%); PCP was not significantly affected. Nifedipine led to significant changes in CI (+9%) and PCP (-34%). The effects of bisoprolol on HR and RPP and of nifedipine on PCP were retained in the combination. Competition was detectable as regards the opposing effects on CI and TPR. Measured by W-ST01 and ST, bisoprolol had a marked anti-ischemic effect, whereas that of nifedipine was distinctly less. There was an increase in effect after combination of the drugs (not significant). In patients with chronic angina pectoris due to coronary artery disease, bisoprolol and nifedipine had different hemodynamic profiles after acute administration; when the two drugs were combined, these effects were partly intensified and partly canceled out. There was a tendency for the effect of bisoprolol to be intensified by nifedipine in the combination. The combination of bisoprolol and nifedipine was well tolerated in the doses selected.
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PMID:Hemodynamics and exercise tolerance after bisoprolol, nifedipine, and their combination in patients with angina pectoris. 1152 30

Serum complement (C3, C4) levels in Libyan patients with acute myocardial infarction (AMI; 31 patients) and angina pectoris (AP; 11 patients) at the 1st day and 7th day of attack were estimated. A group of 26 healthy Libyans were taken as control subjects (CS). Serum C3 and C4 levels (mean +/- SD, mg/dl) were elevated at the 1st day in AMI as well as AP patients (C3 --> AMI1: 154.0 +/- 28.5, AP1: 152.0 +/- 45.0, CS: 132.0 +/- 8.0, ANOVA: p = 0.0072; C4 --> AMII1: 38 +/- 13, AP1: 37 +/- 17, CS: 29 +/- 6, ANOVA: p = 0.0160). No significant differences for the elevated C3 and C4 levels at the 1st day were observed between the two diseases groups (AMI1 vs AP1 --> C3: p = 0.879, C4: p = 0.818). At the 7th day, C3 and C4 levels were further elevated in AMI, while they remained at the similar elevated levels in AP (C3 --> AMI 7: 173.1 +/- 28.0, AP 7: 149.0 +/- 41.0, CS: 132.0 +/- 8.0, ANOVA: p = 0.0000; C4 --> AMI 7: 46.0 +/- 7.0, AP 7: 36.0 +/- 15.0, CS: 29.0 +/- 6.0, ANOVA: p = 0.0000). Again, no significance differences for the raised C3 and C4 levels at the 7th day was observed between AMI and AP patients (AMI 7 vs AP 7 --> C3: P = 0.059, C4: p = 0.06). The C3 elevation showed significant positive correlation in AMI group (r = 0.522, p = 0.003) while it was insignificant in AP patients (r = 0.037, p = 0.915). Regarding C4 levels, it was significantly correlated in AMI (r = 0.483, p = 0.006), and in AP, although it was positively correlated (r = 0.656, P = 0.028) the observed difference was not significant (t = 0.29, p = 0.778). In conclusion, serum C3 and C4 levels were more profoundly elevated in AMI compared to AP patients suggestive of an acute phase and inflammatory response.
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PMID:Serum complement (C3, C4) levels in patients with acute myocardial infarction and angina pectoris. 1878 65