PubMed · 3108290
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D Hager, A M Katz. 1987-06-15. Treating cardiac ischemia: pathophysiologic guidelines.. https://doi.org/10.1080/21548331.1987.11703256
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BACKGROUND: Recent reports suggest a possible link between nifedipine (but not diltiazem) and an increased risk of cancer in patients being treated with calcium antagonists. METHODS: A total of 1054 postmyocardial infarction patients were divided randomly into those being treated with calcium antagonists (n = 566 [nifedipine, 425 patients and diltiazem, 141 patients]) and controls (no calcium antagonist; n = 488). The patients were followed for 26.3 months, and the incidences of cardiac events as well as cancer were compared among the 3 groups. RESULTS: Thirteen patients (2.7%) in the control group developed cancer, whereas 15 patients in the nifedipine group (3.5%; odds ratio, 1.34; 95% confidence interval [95% CI], 0.63-2.85) and 3 patients in the diltiazem group (2.1%; odds ratio, 0.89; 95% CI, 0.27-2.93) developed cancer. CONCLUSIONS: Diltiazem appears to present no increased risk of cancer. The incidence of cancer was slightly higher in the patients receiving nifedipine than in those not being treated with a calcium antagonist, which is consistent with earlier reports; however, this increase was not statistically significant.
Primary pulmonary hypertension is a clinical syndrome with severe pulmonary hypertension where other causal diseases are excluded. The condition is progressive, fatal and disappointingly resistant to therapy. In this article we present three children with the disease. Two of the patients died shortly after diagnosis, one of them during heart catheterization. The third patient showed good response to treatment with calcium channel blockers, diuretics and nightly supplementary oxygen. Quality of life and hemodynamics improved during the first six months of treatment, and remained virtually unchanged for another two years. Her condition then deteriorated rapidly, and she died three years after diagnosis. According to the literature and our experience, investigations with non-invasive methods such as oxygen saturation measurement, echocardiography, and a simple exercise test provide sufficient information to start therapy and monitor therapeutic response. Some patients show vasodilatory response to treatment with drugs, and might benefit from therapy with calcium channel blockers.
1. Whole-cell patch clamp recordings were used to investigate the modulation by reducing and oxidizing agents of recombinant human cardiac L-type Ca2+ channel alpha1C subunits stably expressed in human embryonic kidney (HEK 293) cells. 2. The oxidizing agents thimerosal (10 microM) and p-chloromercuribenzene sulphonic acid (PCMBS; 2 microM to 2 mM) caused irreversible inhibition of Ca2+ channel currents. The reducing agent 1,4-dithiothreitol (DTT; 2 mM) was without effect on Ca2+ channel currents, but reversed the inhibitory actions of thimerosal and PCMBS. 3. Ca2+ channel currents were also inhibited by pretreatment with the methanethiosulphonate compound (2-aminoethyl)methanethiosulphonate (MTSEA, 2.5 mM), but were unaffected by identical pretreatment with (2-sulphonatoethyl)methanethiosulphonate (MTSES, 10 mM). The effects of MTSEA could be fully reversed by DTT (2 mM). The degree of current inhibition caused by 200 microM PCMBS was not significantly affected by pretreatment with MTSEA, and following PCMBS treatment, MTSEA caused a similar degree of inhibition to that observed in cells that were not previously treated with PCMBS. These findings suggested that distinct thiol groups were modulated by these two agents. 4. Hypoxic inhibition of Ca2+ channel currents was unaffected by pretreatment of cells with MTSEA but was fully prevented by treatment with PCMBS. Our results indicate that distinct cysteine residues on the alpha1C subunit can undergo redox modulation and in so doing alter channel function. Some, but not all, of these residues appear to be associated with the mechanism underlying inhibition of this channel by hypoxia.