High blood pressure. Causes, symptoms, treatments

Association between SLCO1B1 -521T>C and -388A>G polymorphisms and risk of statin-induced adverse drug reactions: A meta-analysis.

2017-04-17

Oral provocation tests revealed the relation between long-term oral use of metoprolol and development of psoriasiform and/or eczematous skin lesions in 3 patients. The clinical and histopathological findings in 1 case are described more in detail and are discussed. The data in the recent literature, with respect to side effects of skin due to different beta-blocking agents, are summarized. In addition, some aspects dealing with possible mechanism in the side effects of beta-blocking agents are briefly discussed. Since beta-blocking agents may cause similar side effects, as described during practolol treatment, on should still be alert to this possibility during long-term treatment with (new) beta-blocking agents, which may allow us to prevent serious damage that might occur in different organs.

Carvedilol inhibited cardiac NCX in a concentration-dependent manner in isolated cardiac ventricles, but metoprolol did not. We conclude that carvedilol inhibits NCX1 at supratherapeutic concentrations.

Placebo was given for a run in period of four to six weeks. Metoprolol 100 mg twice daily or atenolol 25 mg twice daily was then given for 16 weeks. The two drugs were then exchanged and treatment continued for a further 16 weeks.

First effects of left ventricular recovery during beta blocker treatment were seen in recordings of longitudinal performance, as expressed by AV plane displacement. Doppler flow dynamics as well as global systolic recovery appeared several weeks later, emphasising the importance of longitudinal performance in evaluating left ventricular function.

In contrast with its effects on enoximone, carvedilol and, to a lesser extent, metoprolol treatment may significantly inhibit the favorable hemodynamic response to dobutamine. No such beta-blocker-related attenuation of hemodynamic effects occurs with enoximone.

Both agents caused bradycardia. Nebivolol caused additionally a decrease in systemic vascular resistance (SVR) and no significant change in pulmonary capillary wedge pressure (PCWP), and cardiac output (CO). In contrast, metoprolol caused a deterioration of LV systolic function characterized by a decrease in cardiac output, and an increase in SVR and PCWP.

As exemplified by the two classes of substance beta blockers and ACE inhibitors, the question is considered as to when new developments within a drug family can be termed innovations and when they must be seen purely as plagiarisms ("me-too" preparations). It is noted that in principle no innovations are to be expected from generics, since these substances are are not the subject of specific research. Although large-scale clinical studies in recent years have identified a new indication--cardiac insufficiency--for the beta blockers metoprolol, bisoprolol and carvedilol, this must not be considered an innovation in the sense of a new development. The translatability of the study results to uninvestigated substances is uncertain. In contrast to the beta blockers, the indications for the ACE inhibitors have long been known, but again, the new generic preparations that have come onto the market are not innovations.

The primary aim of this study was to evaluate the pain relief and tolerability of two pain-relieving strategies in the prehospital phase of presumed acute coronary syndrome (ACS), and the secondary aim was to assess the relationship between the intensity and relief of pain and heart rate, blood pressure, and ST deviation. Patients with chest pain judged as caused by ACS were randomized (open) to either metoprolol 5 mg intravenously (i.v.) three times at 2-min intervals (n = 84; metoprolol group) or morphine 5 mg i.v. followed by metoprolol 5 mg three times i.v (n = 80; morphine group). Pain was assessed on a 10-grade scale before randomization and 10, 20, and 30 min thereafter. The mean pain score decreased from 6.5 at randomization to 2.8 30 min later, with no significant difference between groups. The percentages with complete pain relief (pain score < or = 1) after 10, 20, and 30 min were 11, 16, and 21%, respectively, with no difference between groups. Hypotension was less frequent in the metoprolol group compared with the morphine group (0 vs. 6.3%; P=0.03), as was nausea/vomiting (7.2 vs. 24.0%; P=0.004). At randomization intensity of pain was associated with degree of ST elevation (P=0.009). The degree of pain relief over 30 min was associated with decrease in heart rate (P=0.03) and decrease in ST elevation (P=0.01).In conclusion, in the prehospital phase of presumed ACS, neither a pain-relieving strategy including an anti-ischemic agent alone nor an analgesic plus anti-ischemic strategy in combination resulted in complete pain relief. Fewer side effects were found with the former strategy. Other pain-relieving strategies need to be evaluated.

to demonstrate impact of addition of nicorandil to standard treatment in patients with stable ischemic heart disease (IHD) on clinical manifestations of the disease and safety of conducted therapy.