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PubMed · 4054493

[Hypertrophic gingivitis caused by verapamil].

G Cucchi·S Giustiniani·F Robustelli
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Abstract

We observed gingival hyperplasia, similar clinically to the hyperplasia caused by diphenylhydantoin during the last 11 months in two patients treated by verapamil, suffering from angina pectoris pains. In Case I discontinuation of the calcium antagonist resulted in marked regression of the gingival hyperplasia. Evidence points to a strong relationship between the gingival hyperplasia and the administration of verapamil. Further studies are required to confirm definitively the relationship between the administration of verapamil and gingival hyperplasia, its incidence, and the correlation with local factors.

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Angina PectorisGingivitisHumansHyperplasiaMaleMiddle AgedPhenytoinVerapamilCase ReportsEnglish AbstractJournal Article

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BibTeXRIS

G Cucchi, S Giustiniani, F Robustelli. 1985. [Hypertrophic gingivitis caused by verapamil].. https://pubmed.ncbi.nlm.nih.gov/4054493/

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Effect of a hypoglycemic agent on ischemic preconditioning in patients with type 2 diabetes and stable angina pectoris.

OBJECTIVE: Ischemic preconditioning is an increased tolerance to myocardial ischemia during the second of two consecutive exercise tests. ATP-sensitive K(+) channel blockers, such as glinides and sulfonylurea drugs, can induce loss of ischemic preconditioning. This study aimed to investigate the effects of repaglinide, a hypoglycemic agent with an affinity for myocardial ATP-sensitive K (+)channels, on the results of consecutive exercise tests in patients with diabetes and multivessel coronary artery disease. METHODS: Forty-two patients with type 2 diabetes and chronic stable angina pectoris, and two-vessel or three-vessel disease participated in this study. The patients underwent two consecutive treadmill exercise tests (phase 1). On the day after these exercise tests, 2 mg of oral repaglinide was given to the patients. One week later, two exercise tests were repeated consecutively (phase 2). RESULTS: All patients achieved 1.0-mm ST-segment depression during the four exercise tests (T1, T2, T3, and T4). In phase 2, seven patients improved in time to onset of 1.0-mm ST-segment depression. The worsening of the time to onset of 1.0-mm ST-segment depression in phase 2 demonstrated ischemic preconditioning block in 83.3% of patients (P=0.0001). Even the postexercise electrocardiographic parameters (ST-segment depression morphology and magnitude and arrhythmias) were significantly different between the groups with and without pharmacologic ischemic preconditioning block (P=0.031). CONCLUSIONS: Repaglinide, an oral hypoglycemic agent with ATP-sensitive K(+) channel-blocker activity, eliminated the myocardial ischemic preconditioning in patients with coronary disease and diabetes.

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