Penyakit Jantung KatupProf.Dr.dr Zainal Musthafa. SpJP(K) Jumat, 21-9-2012

Penyakit Jantung Katupdisebabkan al : Penyakit Jantung BawaanRHDHTCAD, dll

Penyakit Jantung Bawaan

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ATRESIA AORTA

STENOSIS PULMONALIS

Demam Rheumatik / Penyakit Jantung Rheumatik (PJR)

Defenisi PJRPenyakit jantung rheumatik (PJR) adalah sebuah kondisi dimana terjadi kerusakan permanen dari katup-katup jantung yang disebabkan oleh demam rheumatik (PDR). Penyakit jantung reumatik merupakan komplikasi yang membahayakan dari demam reumatik

Etiologi Demam rematik biasanya terjadi akibat infeksi streptokokus pada tenggorokanMerupakan suatu reaksi peradangan terhadap infeksi, yang menyerang berbagai bagian tubuh (misalnya persendian, jantung, kulit)

PatogenesisDimulai radang tenggorokan karena infeksi kuman Streptokokus Grup A (> 70 tipe serologi ) yang berupa : radang tenggorokan berat yang khas, dan tidak khas, ataupun tanpa gejala sama sekali. Karena antigen secara imunologi mirip jaringan penyangga manusia, antibodi memberikan reaksi silang dengan jaringan tersebut menimbulkan respon keradangan non-supuratif difus setelah periode laten 1 5 minggu.

EpidemiologiDemam reumatik banyak terdapat pada anak-anak dan orang usia muda (5-15 tahun). Ada dua keadaan terpenting dari segi epidemiologik pada demam reumatik akut ini, yaitu kemiskinan dan kepadatan penduduk, insiden demam reumatik menurun tetapi masih merupakan masalah kesehatan masyarakat di negara-negara berkembang.

Gejala klinis (kriteria Jones 1992)Kriteria MAYORKriteria MINOR

GEJALA MAJORKarditis

Poliartritis: sendi yang terkena secara asimetris, dan peradangan cenderung berpindah dari 1 sendi ke sendi yang lain (poliartritis migratorik), banyak sendi yang terkena memerah, bengkak, hangat & nyeri.

Korea: gerak involunter acak disebabkan terkenanya ganglia basalis pada otak. Berkembang hingga 6 bulan setelah faringitis streptokokus korea dapat menetap selama beberapa minggu, punya prognosis yang baik.

Lesi kulit: eritema marginatum (suatu cincin melingkar eritema yang mengelilingi bagian sentral kulit normal) spesifik pada demam rematik (hanya 10% kasus) penyakit ini berlangsung singkat eritema nodusum(ruam noduler,merah &nyeri tekan secara tipikal terlihat diatas tibia anterior) kurang spesifik, tapi sering terjadi.

Nodul rematik subkutan: di atas penonjolan tulang pada ekstermitas, ukuran sebesar kancing, tidak nyeri dan berlangsung 6-10 minggu. ditis

GEJALA MINOR

Malaise umum, anoreksia, penurunan berat badan, sakit kepala, berkeringat, dan rigor selama 4-8 minggu seringkali dikatakan sebagai virus yang berkepanjangan.Gejala lain berhubungan dengan tromboembolisme sistemik yang mengenai setiap pembuluh darah besar atau deposisi kompleks imun yang menyebabkan cedera vaskular pada kulit, sendi, ginjal, dan sistem saraf pusat(SSP).

Morfologi VegetasiLesi yang patognomonik PDR adalah Badan Aschoff sebagai diagnostik histopatologik. Badan Aschoff ini umumnya terdapat pada septumfibrosa intervaskular, dijaringan ikat perivaskular dan didaerah subendotelial. Pada PJR biasanya terkena ketiga lapisan endokard miokard dan perikard secara bersamaan atau sendiri-sendiri atau kombinasi.

DiagnosisApabila ditemukan 2 kriteria mayor, atau 1 kriterium mayor dan 2 kriteria minor, ditambah dengan bukti adanya infeksi streptokokus sebelumnya, kemungkinan besar menandakan adanya demam rematik

PenatalaksanaanTirah baring dan mobilisasi bertahap sesuai keadaan jantung.Eradikasi terhadap kuman streptokokus dengan pemberian penisillin benzatin.Anti-inflamasi

PencegahanPencegahan primer ditujukan langsung pada streptokokus grup A pada serangan akut, dengan penggunaan obat Penisillinpencegahan sekunder bertujan untuk menghindari terjadinya kekambuhan demam reumatik, maka digunakan pencegahan sekunder yang antara lain dengan pemberian Penisillin G parentral,

Pencegahan Sekunder Sangat Bergantung Pada:

Cara pemberian obat.Keyakinan dan ketaatan pasien dalam pencegahan sekunder ini.Pendidikan orangtua (yang juga merupakan faktor penting akan ketaatan pasien melakukan pencegahan ini).Keadaan sosioekonomi pasien atau keluarganya.Jarak antara tempat tinggal pasien dengan rumah sakit.Manifestasi klinis ketika pasien masuk ke rumah sakit.Kemampuan dokter dan tenaga kesehatan daam mengenali dan melaksanakan pencegahan sekunder ini.

PrognosisPrognosis sangat baik bila karditis sembuh pada saat permulaan serangan akut demam reumatik akut.. Selama 5 tahun pertama perjalanan penyakit, demam reumatik dan penyakit jantung reumatik tidak membaik bila bising organik katup tidak menghilang.

Morfologi VegetasiVegetasi memicu respon peradangan ringan. respon peradangan neutrofilik yang hebat terjadi jika infeksi telah melewati katup avaskular. Embolus sistemik dapat terjadi setiap saat karena sifat vegetasi yang rapuh, dan embolus ini dapat menimbulkan infark, ginjal, miokardium, dan jaringan lain.

DiagnosisDiagnosis ditegakkan berdasarkan gejala-gejalanya, terutama pada orang-orang yang memiliki kecenderungan untuk menderita penyakit ini. Pada ekokardiografi (penggambaran jantung menggunakan gelombang suara) bisa ditemukan adanya vegetasi dan kerusakan katup jantung.

PenatalaksanaanTERAPI ANTIMIKROBA

Terapi Empiris (merencanakan dan memberika terapi tanpa data kultur yaitu sebelum hasil kultur diketahui atau hasil kultur negatif)

Terapi Antimikroba Pasien Rawat Jalan (Pasien-pasien yang memenuhi secara penuh yang memiliki hasil kultur darah steril).

Penyakit Jantung Hipertensi

Classification of hypertension2,15140-159 mmHg systolic 90-99 mmHg diastolic160-179 mmHg systolic100-109 mmHg diastolic >180 mmHg systolic >110 mmHg diastolicThe JNC-7 Report14 combines Grades 2 and 32. Williams B, et al. J Hum Hypertens 2004;18:139-185., 14. Chobanian AV, et al. JAMA 2003;289:2560-2572., 15. ESH Guidelines Committee. J Hypertens 2003;21(6):1011-1053

Why should hypertension be treated? ischaemia myocardial infarction cardiac hypertrophy congestive heart failure stroke TIA (transient ischaemic attack) PRIND (prolonged, reversible, ischaemic, neurological deficit) nephrosclerosis atrophy of nephrons renal failure retinopathy lesions swelling of optic disc blindness

Bradykinin/NOInactive fragments

Angiotensin IAngiotensin IIAT1 RECEPTORAT2 RECEPTORRationale for dual RAS blockade with an ACE inhibitor and ARBVasoconstrictionSodium retentionSNS activationInflammationGrowth-promoting effectsAldosteroneApoptosisVasodilationNatriuresisTissue regenerationInhibition of inappropriate cell growthDifferentiationAnti-inflammationApoptosis

VasodilationTissue protectionAngiotensin II escape

Bradykinin?NO?ACE = angiotensin converting enzyme; ARB = angiotensin II receptor blocker; AT = angiotensin; SNS = sympathetic nervous systemHanon S, et al. J Renin Angiotensin Aldosterone Syst 2000;1:147150; Chen R, et al. Hypertension 2003;42:542547; Hurairah H, et al. Int J Clin Pract 2004;58:173183; Steckelings UM, et al. Peptides 2005;26:14011409

Angiotensin II postsynaptic and presynaptic effectsThe neuro-effector junction1616. Brooks DP, Ruffolo RR. J Hypertens 1999;17(Suppl 2):S27-S32

Interaction between the RAAS and the SNS to control blood pressure

RAS and SNS both control of SBP16RAS = renin-angiotensin system; SNS = sympathetic nervous system; HTN = hypertension; CHF = congestive heart failure; ESRD = end-stage renal disease; CAD = coronary artery disease; LVH = left ventricular hypertrophy16. Brooks DP, Ruffolo RR. J Hypertens 1999;17(Suppl 2):S27-S32

Gestational hypertensionPreeclampsia-eclampsiaChronic hypertensionPreeclampsia superimposed upon chronic hypertension

Endothelial cell dysfunction appears to be the central pathomechanism in the pathogenesis of preeclampsiaFunctions of the endothelium Regulate vascular permeability Regulate vascular cell growth Mediate inflammatory and immune mechanism Modulate lipid oxidation ( metabolic activity )

Endothelial dysfunction

An imbalance between relaxing and contracting factors between anti -and pro-coagulant mediators or growth-inhibiting and growth promoting factors.

Placental ischemiaVery low-density lipoprotein versus toxicity-preventing activityImmune maladaptationGenetic imprintingDeficiency of catechol-O-methyltransferase / 2-methoxyestradiolThe role of RAS

Penyakit Jantung Koroner

Atherogenesis

*Spectrum Of ACSUnstable Angina PectorisAcute Non ST-Elevation Myocardial Infarction (NSTEMI)Acute ST-Elevation Myocardial Infarction (STEMI)

Unstable angina or nonQ-wave MITemporary resolution of instability Future high-risk lesionAcute MIPathophysiology of ACS: Disrupted PlaqueAdapted from Yeghiazarians et al. N Engl J Med. 2000;342:101-114.Plaque ruptureThin capHigh macrophage contentLarge lipid coreIncomplete coronary occlusionComplete coronary occlusionSpontaneous lysis, repair, and wall remodeling

Plaque Disruption Leading to Atherothrombosis FormationAdapted from: Falk E et al. Circulation 1995; 92: 65771.

*Inferior STEMI

*Increased serial cardiac markerTroponin T/Troponin ICKMB

ABBAAThe Tight Stenosis Is Not the Active LesionImages supplied by Steven E. Nissen, MD, Cleveland Clinic.BRupture SiteLipid CoreAtheromaLumen

*

Occluded artery

Penyakit Jantung Katupdisebabkan al : Penyakit Jantung BawaanRHDHTCAD, dll

Penegakan Diagnose al : AnamnesaPemeriksaan FisikPendukung. dll

Tatalaksana al : Non FarmakologiFarmakologiIntervensi / BedahPenyuluhan, dll

Alat EKG

Alat Exersise Test (Treadmill)

Pemeriksaan Ekhokardiografi

Pemeriksaan Ekhokardiografi

Ruangan Lab kateterisasi

Ruangan monitoring kateterisasi

Alat Defibrilator

Alat Defibrilator

********************************This classification system is used by the European and British Societies of Hypertension, and is also generally consistent with the American JNC-7 guidelines*The detection and treatment of high BP and its associated CVD risk should be a key focus of health-care policy, as patients with uncontrolled hypertension can develop serious complications in several end-organ systems, including blood vessels, heart, brain, kidneys and eyes. This diagram summarises some of the end-organ complications and consequences associated with persistent raised blood pressure. Untreated prolonged hypertension puts a strain on the arteries, arterioles and heart, and may have fatal consequences. The first sign of high blood pressure may be end-organ damage, due to damage of small arterioles within the organ.

*Key point: It is hypothesised that, with their different sites of action, dual blockade by angiotensinconverting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) will minimise the counterregulatory effects associated with the use of ACE inhibitors alone, and achieve a more complete inhibitionof the renin-angiotensin system (RAS).

The renin-angiotensin system 1-4ACE inhibitors [Speaker note: Click to build at this point] inhibit the action of ACE and hence there is no production of angiotensin II from angiotensin I, which leads to decreased systemic arteriolar resistance and meandiastolic and systolic blood pressure. Increased concentrations of the vasodilator bradykinin occur because itsdegradation is also inhibited. Through its promotion of nitric oxide (NO) release, bradykinin may contribute to thepositive haemodynamic effects seen with ACE inhibitors. However, ACE inhibition only stops one mechanism for theproduction of angiotensin II. Other pathways e.g. chymase [Speaker note: Click to build at this point] continueto produce angiotensin II and these can lead to a gradual return of angiotensin levels to baseline, a phenomenontermed angiotensin II escape.

Although ACE inhibitors block RAS at the enzymatic level, ARBs [Speaker note: Click to build at this point]specifically inhibit the RAS at the receptor site. AT1 receptor blockers induce a dose-dependent blockade ofangiotensin II-induced effects, resulting in a reduction in blood pressure, cardiac and vascular hypertrophy,proteinuria and glomerular sclerosis. It is postulated that ARBs may provide end-organ protection by blockingangiotensin II via the AT1 receptor, yet leaving the AT type 2 (AT2) receptor unopposed [Speaker note: Click tobuild at this point]. Consequently, any circulating levels of angiotensin II will activate the AT2 receptor (amongother subgroups of AT receptors; currently, four are known), which can mediate increases in renal interstitial fluidbradykinin concentrations. Thus, co-administration of an ARB may enhance vasodilatory effects by independentlypotentiating the increase in bradykinin levels observed with ACE inhibitor treatment.5

It is hypothesised that, with their different sites of action, dual blockade by ACE inhibitors and ARBs will minimisethe counter-regulatory effects associated with the use of ACE inhibitors alone, and achieve a more completeinhibition of RAS.

References Hanon S., et al. Persistent formation of angiotensin II despite treatment with maximally recommended doses of angiotensin converting enzyme inhibitors in patients with chronic heart failure. J Renin Angiotensin Aldosterone Syst 2000;1:147150. Hurairah H. & Ferro A., The role of the endothelium in the control of vascular function. Int J Clin Pract 2004;58:173183. Chen R., et al. Important role of nitric oxide in the effect of angiotensin-converting enzyme inhibitor imidapril on vascular injury. Hypertension 2003;42:542547. Steckelings U.M., et al. The AT2 receptor matter of love and hate. Peptides 2005;26:14011409. Siragy H.M., et al. Angiotensin-converting enzyme inhibition potentiates angiotensin II type 1-receptor effects on renal bradykinin and cGMP. Hypertension 2001;38:183186.

*There is growing evidence supporting the concept that angiotensin II can regulate the amount of norepinephrine released from peripheral sympathetic neurones. Animal studies indicate that it does this by stimulating angiotensin II type 1 (AT1) receptors located on the presynaptic nerve terminal of sympathetic neurones, and this triggers enhanced release of norepinephrine into the synapse. This is in addition to its effects on AT1 receptors located postsynaptically on blood vessels, which trigger its direct vasoconstrictor effects.**The renin-angiotensin system (RAS) and sympathetic nervous system (SNS) play important interlinked roles in the control of systolic blood pressure. Angiotensin II and norepinephrine are both powerful vasoconstrictors with direct effects on peripheral resistance. They also appear to affect vascular growth, which contributes to arterial stiffening and compliance.

Interactions between the RAS and SNS occur on several levels. The SNS can affect the release of renin and the subsequent formation of angiotensin II, whilst angiotensin II may alter sympathetic outflow within the brainstem and can modulate the release of norepinephrine from presynaptic neurones.

This diagram summarises the impact of the sympathetic nervous system (SNS) and renin-angiotensin system (RAS) on systolic blood pressure and cardiovascular disease.**********N0-188 Prevent Slide Kit **Disruption of an atherosclerotic plaque is a complex pathophysiologic process central to the initiation of the acute coronary syndromes (ACS). A mature plaque is made up of 2 main components: a lipid-rich core and extracellular matrix proteins forming a fibrous cap. The presence of large, eccentric lipid pools and the infiltration of foam cells are features most often associated with plaque rupture or fissure, which usually occurs at the sites of the greatest mechanical stress. Fissures that occur at weak cap sites not under great mechanical stress are thought to be initiated by enzymatic degradation of the cap. Local thrombosis following plaque disruption results from interactions between the lipid core and blood.Numerous factors probably trigger the rupture of a vulnerable plaque. Rupture exposes tissue factor in the lipid core, which precipitates platelet activation, adhesion, and aggregation, resulting in the formation of an occlusive thrombus. If the process leads to complete occlusion of the artery, an acute MI results. Alternatively, if occlusion is incomplete, unstable angina or nonQ-wave MI may develop. Spontaneous or pharmacologic lysis of thrombus, or pharmacologic interruption of platelet aggregation, may lead to resolution of the syndrome.Slide 16Yeghiazarians Y, Braunstein JB, Askari A, Stone PH. Unstable angina pectoris. N Engl J Med. 2000;342:101-114.*The hemostatic process to form a thrombus is not uniform size and composition of the blood clot varies with the site of injury. The result of plaque rupture and consequent thrombus formation can therefore be an acute event (such as myocardial infarction), or contribute to the long-term underlying progression of vascular disease.A large fissure typically results in the formation of a large thrombus that completely occludes the vessel resulting in an acute vascular event.A smaller fissure may result in a mural thrombus that partially or transiently occludes the artery, causing acute ischemia and contributing to the progressive process of plaque growth.Reference:1. Falk E et al. Circulation 1995; 92: 65771.**N0-188 Prevent Slide Kit **Intravascular ultrasound (IVUS) imaging documents the thickness and composition of plaque in the arterial wall, and will show diffuse disease. In these views, IVUS is compared with angiography to show that tight stenosis is not necessarily the site of an active plaque. The small lumen seen at A on the angiogram represents a stenosis that is significant but without rupture. However, the hazy area at B on the angiogram contains a ruptured plaque with an exposed lipid core, as seen on the corresponding IVUS image.Slide 15*************Slide*Slide*Slide**