Somo 1Uundaji wa arrhythmia ya atria na thromboembolism katika atrial fibrillation sugu: remodeling ya atria, stasis, na hatari ya kiharusiInaelezea jinsi ugonjwa wa atrial fibrillation sugu unavyobadilisha muundo na utendaji wa atria, kukuza kusimama kwa damu, na kuongeza hatari ya thromboembolism, ikichanganya biolojia ya remodeling na utabiri wa kiharusi kliniki, picha, na mikakati ya anticoagulation.
Electrical and structural atrial remodelingLoss of atrial kick and hemodynamic impactLeft atrial appendage stasis and clotCHA₂DS₂-VASc and bleeding risk scoresImaging of atrial thrombus and flowPathophysiology of cardioembolic strokeSomo 2Pathofiziolojia ya ischemia katika infarction ya myocardial yenye kunyanyuliwa kwa ST (STEMI): kupasuka kwa plaque, thrombosis, infarction ya transmural na anatomia maalum ya ukuta wa chiniInashughulikia mfululizo kutoka kupasuka kwa plaque hadi kufungwa kwa thrombosis na infarction ya transmural katika STEMI, ikisisitiza anatomia ya coronary, udhaifu wa ukuta wa chini, ushiriki wa ventricular ya kulia, na maana kwa dalili, ECG, na tiba.
Plaque rupture and thrombosis cascadeComplete occlusion and wavefront necrosisTransmural injury and ST-elevation patternsInferior wall blood supply and variantsRight ventricular infarction physiologyReperfusion injury and salvageable myocardiumSomo 3Mwingiliano wa magonjwa ya kawaida (shinikizo la damu, kisukari, CKD, kiharusi kilichopita, sigara, hyperlipidemia) na pathofiziolojia ya moyoInachanganya jinsi shinikizo la damu, kisukari, CKD, kiharusi kilichopita, sigara, na hyperlipidemia zinavyoingiliana na muundo wa moyo, mishipa, na hemostasis, kuharakisha atherosclerosis, remodeling, arrhythmias, na maendeleo ya kushindwa kwa moyo.
Hypertension and pressure overload LVHDiabetes, microvascular disease, and HFCKD, uremic toxins, and volume overloadHyperlipidemia and atherosclerotic burdenSmoking, endothelial injury, and thrombosisPrior stroke and cardio-cerebral interplaySomo 4Mapungufu ya miundo ya pathofiziolojia na tafsiri kwa wagonjwa wenye multimorbidity na umri mkubwaInajadili kwa nini miundo ya pathofiziolojia ya kawaida inaweza kushindwa katika watu wazima wakubwa na wagonjwa wa multimorbidity, ikiangazia akiba iliyobadilishwa, polypharmacy, udhaifu, na hatari zinazoshindana zinazofanya utambuzi, utabiri wa hatari, na uchaguzi wa matibabu ugumu.
Physiologic aging and reduced reserveAtypical presentations in older patientsMultimorbidity and competing mechanismsPolypharmacy and altered drug responseRisk scores in heterogeneous populationsIndividualizing goals and shared decisionsSomo 5Taratisibu za dawa: ACEi/ARB/ARNI, beta blockers, MRAs, SGLT2 inhibitors, antiplatelet na wakala wa anticoagulant, tiba za reperfusion na athari zao za fiziolojiaInapitia taratibu za madawa ya aina kuu za moyo, ikiangaza malengo ya receptor na njia za signaling kwa athari za hemodinamiki, neurohormonal, na antithrombotic, na kuelezea jinsi hizi zinavyotafsiriwa kuwa faraja ya dalili na faida za matokeo.
RAAS blockade with ACEi, ARB, and ARNIBeta-blockers and sympathetic modulationMRAs and aldosterone-driven remodelingSGLT2 inhibitors and cardiorenal effectsAntiplatelet pathways and platelet inhibitionAnticoagulants and coagulation cascade targetsSomo 6Matokeo ya hemodinamiki ya LVEF iliyopungua: preload, afterload, contractility, na congestion inayeelezea dyspnea, orthopnea, JVP, crackles, edemaInaelezea jinsi kupungua kwa ejection fraction ya ventricular ya kushoto kunavyobadilisha preload, afterload, na contractility, kutoa congestion na pato la chini, na kuunganisha mabadiliko haya na dalili za kitanda kama dyspnea, orthopnea, kunyanyuliwa kwa JVP, crackles, na edema.
Frank–Starling curve in systolic failureAfterload, arterial tone, and LV performanceNeurohormonal responses to low outputPulmonary venous hypertension and dyspneaSystemic venous congestion and edemaJVP, hepatojugular reflux, and exam cluesSomo 7Msingi wa fiziolojia kwa matokeo ya vipimo vya utambuzi: mabadiliko ya ECG (LVH, kunyanyuliwa kwa ST cha chini, AF), matokeo ya echo katika HFrEF na abnormalities za mwendo wa ukuta, biomarkers (troponin, BNP/NT-proBNP)Inachunguza jinsi fiziolojia ya moyo inavyotengeneza mifumo ya ECG, echocardiographic, na biomarker, ikiwezesha wanafunzi kutafsiri LVH, ischemia, atrial fibrillation, na matokeo ya kushindwa kwa moyo kwa njia ya kinadharia, yenye manufaa kliniki.
Voltage criteria and repolarization in LVHInferior ST-elevation and coronary anatomyAF mechanisms and ECG irregularityEcho features of HFrEF and wall motionTroponin kinetics and myocardial necrosisBNP/NT-proBNP and wall stress physiologySomo 8Remodeling ya moyo na taratibu za kushindwa kwa systolic zinazoongoza kwa kushindwa kwa moyo wenye ejection fraction iliyopungua (HFrEF)Inaelezea michakato ya kimolekuli, seli, na muundo inayoendesha remodeling ya moyo na kushindwa kwa systolic katika HFrEF, ikijumuisha uanzishaji wa neurohormonal, jeraha la myocyte, fibrosis, na upanuzi wa chumba, na jinsi mabadiliko haya yanavyozidisha utendaji wa pampu.
Myocyte loss, apoptosis, and necrosisHypertrophy, dilation, and geometry changeFibrosis, stiffness, and conduction delayNeurohormonal drivers of remodelingMitral regurgitation from LV dilationReverse remodeling with guideline therapy