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Successful treatment with sildenafil in systemic sclerosis patients with isolated pulmonary arterial hypertension: two case reports.

Hayakawa I, Shirasaki F, Hirano T, Oishi N, Hasegawa M, Sato S, Takehara K.

Department of Dermatology , Kanazawa University Graduate School of Medical Science , 13-1 Takaramachi , Kanazawa, Ishikawa, 920-8641, Japan, shirasah@med.kanazawa-u.ac.jp.

We describe two systemic sclerosis (SSc) patients with isolated pulmonary arterial hypertension (PAH) who were given treatment with 50 mg oral sildenafil per day. We evaluated the efficacy of oral sildenafil for isolated PAH in SSc patients by direct assessment with cardiac catheterization before and 6 months after the initiation of sildenafil. Right-heart catheterization demonstrated decreased mean pulmonary artery pressure, decreased pulmonary vascular resistance, and increased cardiac output after treatment with sildenafil. Brain natriuretic peptide levels were gradually decreased. The 6-min walking distance was greatly extended. Moreover, the physical conditions of both patients were much improved. We recognized no adverse events. We propose that oral sildenafil may be beneficial as a selective pulmonary vasodilator and as long-term treatment in SSc patients with isolated PAH.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15915331&query_hl=1

Acute Myocardial Infarction After Sildenafil Citrate Ingestion (July/August).

Kekilli M, Beyazit Y, Purnak T, Dogan S, Atalar E.

Department of Internal Medicine, Hacettepe Medicine Faculty, Ankara, Turkey.

OBJECTIVE: To report a case of acute myocardial infarction (MI) associated with the use of oral sildenafil in a nitrate-free patient. CASE SUMMARY: A 45-year-old man was admitted to the hospital with acute left-sided chest pain, nausea, and vomiting that started approximately 30 minutes after taking sildenafil 100 mg before a sexual contact. The patient was diagnosed with an acute anterior MI, and therapy with aspirin, metoprolol, and unfractionated heparin was initiated. Early coronary reperfusion treatment with primary percutaneous transluminal coronary angioplasty was performed after initial evaluation. Balloon angioplasty followed by coronary stenting was performed successfully in the 80%-occluded left anterior descending artery. The patient was discharged one week after the coronary intervention without complication. DISCUSSION: Sildenafil-associated MI is rarely seen in patients without documented coronary artery disease. By inhibiting phosphodiesterase type 5, sildenafil can cause an increase in cyclic guanosine monophosphate levels, which mediates the relaxation of vascular smooth muscle in the corpus cavernosum. Although sildenafil can cause a major decline in systemic arterial pressure in the existence of organic nitrates, physicians should be aware of its adverse cardiovascular effects even in nitrate-free patients. The Naranjo probability scale indicates that sildenafil was the possible cause of the MI. CONCLUSIONS: Sildenafil may rarely be associated with MI in patients with no known cardiac history. Physicians should be aware of this rare and serious adverse reaction to sildenafil and counsel patients not to take sildenafil before undergoing a complete physical evaluation and further testing if warranted.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15914518&query_hl=1

Involvement of the NMDA receptor, NO-cyclic GMP and nuclear factor K-beta in an animal model of repeated trauma.

Harvey BH, Bothma T, Nel A, Wegener G, Stein DJ.

School of Pharmacy (Pharmacology), Faculty of Health Sciences, North-West University, Potchefstroom, South Africa, 2520.

Post-traumatic stress disorder (PTSD) may be associated with shrinkage of the hippocampus, with glutamate release causally related to these events. Recent animal studies strongly implicate activation of the nitric oxide (NO)-cascade in anxiety and stress. Using an animal model of repeated trauma, the effect of stress was investigated on the hippocampal NO-cGMP signalling pathway, specifically the release of nitrogen oxides (NOx) and its modulation by NMDA receptor-, NO-, cGMP- and nuclear factor K-beta (NFK-beta)-selective drugs. Immediately after stress, rats received the glutamate NMDA receptor antagonist, memantine (MEM; 5 mg/kg i.p./d), the NO synthase inhibitor, 7-nitroindazole sodium salt (7-NINA; 20 mg/kg i.p./d), the cGMP-specific PDE inhibitor, sildenafil (SIL; 10 mg/kg i.p./d) or the NFkappa-beta antagonist, pyrollidine dithiocarbamate (PDTC; 70 mg/kg i.p./d), for 7 days. Stress significantly increased hippocampal NOx on day 7 post-stress, which was blocked by either 7-NINA or PDTC, while MEM was without effect. SIL, however, significantly augmented stress-induced NOx accumulation. Increased cGMP therefore acts as a protagonist in driving stress-related events, while both nNOS (neuronal NOS) and iNOS (inducible/immunological NOS) may represent a therapeutic target in preventing the effects of severe stress. The value of NMDA receptor antagonism, however, appears limited in this model. Copyright (c) 2005 John Wiley & Sons, Ltd.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15912566&query_hl=1

Pulmonary hypertension: inhaled nitric oxide, sildenafil and natriuretic peptides.

Steiner MK, Preston IR, Klinger JR, Hill NS.

Pulmonary, Critical Care and Sleep Divisions, Tufts-New England Medical Center, Boston, Massachussets, USA.

Phosphodiesterase-5 (PDE5) inhibitors and other agents that modulate intracellular cGMP are now emerging as promising, safe, and easy to administer therapies for pulmonary hypertension, with relatively few side effects. Recent studies have shown that PDE5 inhibitors are potent acute pulmonary vasodilators in experimental models that partially reverse established pulmonary arterial hypertension and blunt chronic pulmonary hypertension. In addition, studies on animals reveal that PDE5 inhibitors work in concert with nitric oxide and/or natriuretic peptide levels by enhancing intracellular cGMP and cGMP-mediated vasodilator effects. Further, the combination of PDE5 inhibitors and agents that increase cGMP or cAMP also yields additive beneficial effects on pulmonary hemodynamics in patients with pulmonary arterial hypertension.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15907910&query_hl=1