JADWAL JAGA PPDS PER AGUSTUS 2012

PENATALAKSANAAN PASIEN DENGAN SEVERE PULMONARY HYPERTENSION & GAGAL JANTUNG KANAN

Andri Eko Purnomo, Mohammad Yogiarto

Terdapat kemajuan dalam terapi medis, tetapi Pulmonary Arterial Hypertension (PAH) terus menyebabkan morbiditas dan mortalitas yang signifikan. Meskipun ventrikel kanan dapat beradaptasi dengan peningkatan afterload, perkembangan vasculopathy paru sebagai ciri Pulmonary Arterial Hypertension menyebabkan banyak pasien mengalami kegagalan ventrikel kanan yang progresif. Selanjutnya, dekompensasi ventrikel kanan akut bisa terjadi akibat dari meningkatkan kebutuhan jantung secara akut, seperti sepsis, atau meningkatnya afterload ventrikel, termasuk gangguan dalam terapi medis, aritmia, atau emboli paru. Sedikitnya cadangan dari ventrikel kanan, iskemia ventrikel kanan, dan pengaruh efek samping ventrikel kanan pada pengisian ventrikel kiri dapat menyebabkan penurunan global dalam distribusi oksigen dan kegagalan multi organ. Hanya sedikit data yang menjadi pedoman bagi dokter untuk merawat gagal jantung kanan akut pada Pulmonary Arterial Hypertension. Rekomendasi pengobatan sering didasarkan pada model binatang dengan gagal jantung kanan akut atau pada manusia dengan pulmonary  hypertension karena berbagai sebab. Keberhasilan pengobatan sering membutuhkan hemodinamik invasif yang digunakan untuk memantau efek biologis.

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JADWAL PEMBAYARAN SPP SEMESTER BARU PER JULI 2012

Pembayaran SPP dapat dilakukan mulai tanggal  23 JULI 2012 s.d 23 AGUSTUS 2012

DIAGNOSIS DAN PENATALAKSANAAN KARDIOMIOPATI ALKOHOLIK

Mauliana Budiastuti, Dyah Priyatini

Long-term heavy alcohol consumption is the cause of a nonischemic, dilated cardiomyopathy, herein referred to as alcoholic cardiomyopathy (ACM). ACM is a specific heart muscle disease of a known cause that occurs in two stages: an asymptomatic stage and a symptomatic stage. In general, alcoholic patients consuming > 90 g of alcohol a day (approximately seven to eight standard drinks per day) for > 5 years are at risk for the development of asymptomatic ACM. Those who continue to drink may become symptomatic and develop signs and symptoms of heart failure. ACM is characterized by an increase in myocardial mass, dilation of the ventricles, and wall thinning. The pathophysiology of ACM is complex and may involve cell death (possibly due to apoptosis) and changes in many aspects of myocyte function. Alcohol abstinence, as well as the use of specific heart failure pharmacotherapies, is critical in improving ventricular function and outcomes in ACM.

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JADWAL DPJP KARDIOLOGI JULI 2012

JADWAL JAGA PPDS KARDIOLOGI JULI 2012

CARDIOVASCULAR RISK in POSTMENOPAUSAL WOMEN

Mutiara Rizki Haryati, M. Djoko Soemantri

Menopause is a universal and irreversible part of the overall aging process which involves a woman's reproductive system. Menopause results from loss of ovarian sensitivity to gonadotropin stimulation, which is directly related to follicular decline and dysfunction causing decrease in estrogen level. Coronary artery disease is the leading cause of morbidity and mortality in men and postmenopausal women. Menopausal status increases the cardiovascular risk for women independent of age whereas natural menopause not causes an immediate increase in risk of heart disease. Cardiovascular risk factors changes occurring with menopause have been considered the biological mechanism. The risk-factor prevalence increases with advancing age and varies widely by country. Deprivation of endogenous estrogen is assumed to be a crucial factor in the increasing cardiovascular risk. Interaction of high blood pressure with other risk factors is particularly important in case of postmenopausal women. Several studies have demonstrated that lipid concentrations, body weight, blood pressure, and insulin resistance increase after menopause which may impair endothelial functions. The state of “endothelial activation,” is characterized by a proinflammatory, proliferative, and procoagulatory status that favours atherogenesis. Both inflammatory processes and a disturbed lipid profile may mediate the development and progression of atherosclerosis. We focused on the relationship between hormonal status and cardiovascular risk assessed by inflammatory markers and traditional laboratory variables in women during postmenopausal status.

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