Cardiovascular Journal of Africa: Vol 26 No 6 (November/December 2015)

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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 26, No 6, November/December 2015 AFRICA 213
80(2–3): 257–259.
7. Walia HS, Walia SS, Emanuel ME. Sick sinus syndrome associated with
topical timolol maleate instillation. J Pharmacol Pharmacother 2011;
2(4): 300–302. doi: 10.4103/0976-500X.85946.
8. Rubín López JM, Hevía Nava S, Veganzones Bayón A, Barriales
Alvarez V. Atrioventricular block secondary to topical ophthalmic beta
blockers. Rev Esp Cardiol 1999; 52(7): 532.
9. Anguita M, Torres F, Giménez D, Segura J, Aumente D, Suárez de Lezo
J, et al. Bradyarrhythmias secondary to the use of ophthalmic timolol.
A report of 3 cases. Rev Esp Cardiol 1992; 45(1): 71–73.
10. Rosen KM, Gunnar RM, Rahimtoola SH. Site and type of second
degree AV block. Chest 1972; 61: 99–100.
11. Rardon DP, Miles WM, Zipes DP, eds. Atrioventricular Block and
Dissociation. Philadelphia, PA: WB Saunders Co, 2000.
12. Narula OS, Samet P. Wenckebach and Mobitz type II AV block due to
block within the His bundle and bundle branches. Circulation 1970; 41:
947–965.
13. Langerdorf R, Cohen H, Gozo EG. Observations on second degree
atrioventricular block, including new criteria fort the differential diag-
nosis between type I and type II block. Am J Cardiol 1972; 29: 111–119.
14. Edwards IR, Aronson JK. Adverse drug reactions: definitions, diagno-
sis, and management. Lancet 2000; 356(9237): 1255–1259.
15. Zeltser D, Justo D, Halkin A, Rosso R, Ish-ShRalom M, Hochenberg
M, et al. Drug-induced atrioventricular block: Prognosis after discon-
tinuation of the culprit drug. J Am Coll Cardiol 2004; 44:105–108.
16. Osmonov D, Erdinler I, Ozcan KS, Altay S, Turkkan C, Yildirim E, et
al. Management of patients with drug-induced atrioventricular block.
Pacing Clin Electrophysiol 2012; 35(7): 804–810.
17. Neufeld AH, Bartels SP. Receptor mechanisms for epinephrine and
timolol. In: Lutjen-Drecoll E, ed. Basic Aspects of Glaucoma Research .
Stuttgart, Germany: Schattauer, 1982: 113–122.
18. Hopkins GA, Lyle WM. Potential systemic effects of six common
ophthalmic drugs. J Am Optometric Assoc 1977; 48: 1241–1245.
19. Korte JM, Kaila T, Saari KM. Systemic bioavailability and cardio-
pulmonary effects of 0.5% timolol eye drops. Graefes Arch Clin Exp
Ophthalmol 2002; 240: 430–435.
20. Salminen L. Review: systemic absorption of topically applied ocular
drugs in humans. J Ocul Pharmacol 1990; 6: 243–249.
21. Quaranta L, Miglior S, Floriani I, Pizzolante T, Konstas AG. Effects of
the timolol–dorzolamide fixed combination and latanoprost on circa-
dian diastolic ocular perfusion pressure in glaucoma. Invest Ophthalmol
Vis Sci 2008; 49(10): 4226–4231.
22. Quaranta L, Gandolfo F, Turano R, Rovida F, Pizzolante T, Musig A,
et al. Effects of topical hypotensive drugs on circadian IOP, blood pres-
sure, and calculated diastolic ocular perfusion pressure in patients with
glaucoma. Invest Ophthalmol Vis Sci 2006; 47(7): 2917–2923.
23. Fraunfelder FT, Meyer SM. Systemic adverse reactions to glaucoma
medications. Int Ophthalmol Clin 1989; 29(3): 143–146.
24. Orzalesi N, Rossetti L, Omboni S; OPTIME Study Group (Osservatorio
sulla Patologia glaucomatosa, Indagine Medico Epidemiologica);
CONPROSO (Collegio Nazionale dei Professori Ordinari di Scienze
Oftalmologiche). Vascular risk factors in glaucoma: the results of
a national survey. Graefes Arch Clin Exp Ophthalmol 2007; 245(6):
795–802.
Increased platelet activation leads to cardiovascular risk in
adolescents with type 2 diabetes
Adolescents with type 2 diabetes are at risk of atherosclerosis
and cardiovascular disease early on in life. There are well-
established data that diabetes, platelet hyperactivity and
cardiovascular disease (CVD) are causes of mortality in
adults with type 1 and type 2 diabetes.
The purpose of a pilot study by Israels et al., published in
Diabetes Care on 4 June 2014, was to establish whether the same
connection was present in adolescents as in adults relative to
non-diabetic control subjects. The study examined the expression
of the surface and soluble platelet activation markers.
In vivo platelet activation was compared in four different
groups of adolescents aged 12 to 18 years. These groups
comprised type 1 diabetics (n = 15), type 2 diabetics ( n =
15), control subjects with normal body mass index (n = 14)
and control subjects who were obese/overweight (n = 13).
Type 1 and 2 diabetes were classified according to Canadian
Diabetes Association criteria.
Subjects with Prader–Willi syndrome or hypothyroidism,
those who abused alcohol or drugs, had congenital CVD,
were pregnant, and/or who used glucocorticoids, lipid-
lowering agents or platelet-inhibitory agents were all excluded
from this study.
Measurements of platelet surface and soluble activation
markers were performed using the FACSCalibur flow
cytometer. Results were shown as percentage of platelets
expressing CD62P and CD63 platelet surface antigen as well
as PAC-1 monoclonal antibodies.
Results showed that there were significantly higher
platelet activation markers in adolescent type 2 diabetics
when compared with either the obese or normal control
group (p < 0.05). There was a small difference in platelet
activation between adolescent type 1 diabetics and the two
control groups, although the pattern leaned towards an
increase in activation markers for type 1 diabetics. There
were no differences in platelet activation markers between the
non-diabetic groups.
The study showed that in vivo platelet activation was
increased in adolescent type 2 diabetics, which can be a
potential cause of atherosclerosis, thrombosis and other
cardiovascular diseases in early adulthood. Although it was
a small study, it raises awareness of the fact that a more
aggressive approach should be undertaken when modifying
therapeutic interventions for type 2 diabetes in adolescents.
Reference
platelet-activation-leads-to-cv-risk-in-adolescents-with-type-2-diabetes