84, IHD, LSHF, RSHF

IHD:
Group of syndromes related to myocardial ischemia.
- Imbalance between supply and demand of oxygen to heart.
- Poor supply: anaemia or CO poison.
- Incr. demand: incr. HR and HT
- Most common cause is CAD
- CAD is caused by a combo. of atherosclerotic plaque, superimposed thrombus
and vasospasm
- Commonly affected are the LAD, LCA, RCA
- 75% blockage: angina on exertion, 90% blockage: pain at rest
- Rate of blockage development is important: Sudden causes inevitable damage,
Steady allows adaptation

LSHF:
- Failing LV, leads to pulm. cong. and insuff. periph. blood supply
- Generally: LV hypertrophy and dilated (except.: mitral valve stenosis)
- 2ndry LA enlarg. cause atrial fibrillation (decr. SV and incr. thrombosis)
- Pulm. cong. leads to pulm. oedema (see heart failure cells) [Histo. 18]
- CF: dyspnea, cough, orthopnea, cardiomegaly

RSHF:
- Usually, conseq. of LSHF: pressure incr. in pulm. circ. cause pres. incr.
in RV/RA
- Causes: isolated RSHF for disease of lung parenchyma, Cor pulmonale, rightleft shunt (congenital)
- Cong. of liver, portal HT, oedema of bowel and ascites, pleural effusion,
peripheral oedema (lower limb), anasarca

85, Angina. Acute coronary syn.

Angina def.: Chest pain caused by short lasting, reversible myocardial
ischemia
- Causes: obstruction or spasms of coronaries
- Three types:
Stable: episdoic chest pain ass. w/ excercise or increased O2 demand of
heart (tachy. and HT due to fear). About 75% occlusion of coronary, enough
for rest, but not for exertion.
Unstable: incr. freq. of pain, with little to no excercise. Conseq.
episodes are longer and more intense. Ass. w/ plaque with superimposed
thrombosis, or distal embolisation w/ vasospasm. High risk for infarct,
therefore also named pre-infarction ischemia.
Variant (prinzmetal): Pain at rest due to CA vasospasm.
ACS def.: Any group of symp. ass. w/ obstruction of coronaries.
e.g chest pain rad. to left arm & jaw, nausea, sweating.
- Ass. w/ angina.
- May result from: STEMI, Non STEMI, Unstable angina
- SCD is ass. w/ ACS
- SCD def.: Unexpected death from cardiac causes within short time of
(known/unknown) cardiac disease. [V-fib is ultimate mech. of SCD]

86, Etiology, PG & morph. of MI

MI def.: Necrosis of cells of the myocardium due to O2 deprivation.
- Freq. incr. w/ age., (other factors: smoking, HT, DM), M>F
- PG: (most) acute CA thrombosis from rupture of atherosclerotic plaque w/
superimposed thrombosis.
- CA occlusion events:
Plaque rupture, exposure of sub. endo. collagen and necrotic cont.,
platelet agg. and act., release 2ndry aggregators (TXA2, ADP, Serotonin),
mediators stim. vasospasm, Extrin. PW of coagulation, thrombus formation.
- Myocardial response to isch.: aerobic resp. stops, anaerobic resp. begins,
acc. of lactic acid other BD products. Isch. may cause arrhthymias, thus SCD.
- Mild isch. (first 20 mins.): revers. damage of myocytes. Loss of
contractility, reperfusion may save cells.
- Sever isch. (20-40 mins.): irrevers. damage/death of myocytes. Coag.
necrosis. Sub-endmyo. first, then outwards. Prolonged isch. leads to
transmural death of myocytes.
- Extent of damage depends on: [location, timing, severity of CA occlu.],
which CA, duration of occlu., O2 demand.
- Morph: 50% of MI in LV or IV septum. Affected CA [LAD 50%, RCA 35%, LCA
15%].
First 12hrs: coag. necr., w/n 1 week: loss of spec. architecture
(striations) and phagocytosis, w/n 2 weeks: granulation tissue, w/n 2 months:
scar form.
- Reperfusion: thrombolysis, balloon angioplasty, bypass. Restore blood flow.
Complications: more damage, free radical form. (microvascular injury),
hemorrhage (leaky vasculature).
Myocardial stunning: revers. decr. in contractility after reperfusion.

87, HT. Cor pulmonale.

HT:
- Systemic HT heart caused by: LV hypertrophy (w/o other CV disease), and
family history of HT.
- Prolonged HT (140/90) causes LV hypertrophy. No dilation. Incr. wall
thickness impairs diastolic filling, 2ndry LA enlargement.
Wall thickness: 2cm, Heart weight: >500g
Cor pulmonale def.: abn. enlarg. of right heart due to pulm. HT
- Pulm. HT can be caused by 1ry disorder of lung parenchyma or pulm.
vasculature
- RV hypertrophy can be congenital, or b/c LSHF [# 84]
- Acute or chronic
Acute CP: due to massive PE (>50% occlu.), RV dilated w/o hypertrophy.
Chronic CP: prolonged pulm. HT (emphysema, fibrosis, 1ry pulm. HT). RV
hypertrophy. Pulm. art. may cont. atherosclerotic plaques (not norm.!!!)

88, Rheumatic fever. Rheumatoid heart disease.

RF:
- Acute, immune mediated, multisystem inflamm. dx
- Few wks. after infec. from Group A beta-hemolytic strep. pharyngitis.
- Acute rheumatoid heart dx.: cardiac manif. of RF. Inflamm. of valves,
myocard., or pericard. Chron. valve damage leads to diffuse and dense
scarring, permanent dysfunction, mitral stenosis.
- Morph:
Acute RF heart: Aschoff bodies, Anitschkow cells (activated MP with
much cyto., central nuclei, wavy chromatin (like a caterpillar). Valve has
fibrinoid necrosis.
Chronic RF heart: Organised acute form leads to scarring. Mitral valve
leaflet thickened. Corda tendinae short, thick and fused. Aschoff bodies
replaced wit scars.
Result: valvular stenosis (RF causes 99% of mitral stenoses in the world).
70% RF cause mitral (bicusp.) stenosis. 30% RF cause tricuspid stenosis.
- PG: Acute RF is HSR type II. AB for strep cross-react with host-AG in
heart, joints, others. 2-3wks after infec. No bact. on lesions.
- CF: Mostly children (5-15yrs). Main sx: carditis (children), arthritis
(adults). Patients more vulnerable to reactivation after pharyngeal infec.

89, Valvular stenosis & insuff. Mitral valve prolapse.

Valvular stenosis:
- Def.: Valve fails to open completely, obstructs forward flow.
- Chronic process, 1ry cuspal ab. (calcification or scar)
- 2/4 of all acq. sten are mitral or aortic valve.
- Valves degen. with age (calcification and scar), calcification on outflow
side.
- Calcified aortic sten.: Most common degen. valvular dx., MCC of aortic
stenosis. Normally starts in 70s. Calc. fills sinus of Valsalva/aortic sinus
(see images), valve can't open.
- Mitral valve calc.: calc. of edge of leaflets, norm. asymptomatic (unless
interferes with conduc.)
- CF of stenosis: can be comp. by 70-80%. LV outflow obs. Incr. pressure in
LV (upto 200mmHg). CO maintained by LV hypertrophy. Mild isch, develop
angina. Fainting if not enough blood to brain.
Valvular insuff.:
- Def.: valve fails to close completely, allows reversed flow.
- Result of intrinsic disease of cusps, or distortion of supporting
structures (e.g. aorta, mitral annulus, chorda tendinae, pap. musc.)
Mitral valve prolapse:
- One or both valves are floppy, prolapse back into LV during systole.
- F>M (x7)
- Affected leaflets: big, thick, rubbery
- Corda tendinae: elong., thin, ruptured (sometimes)
- Morph: thinning of the fibrosa layer (resp. for the valve's strength)
- CF: most asymptomatic, it is found by accident.

90, Infect. and non-infect. endocarditis

IE:
- Serious infec., needs quick diag. and treat.
- Microbial invasion of valves or endocard., causes destruction of tissue and
creates ab. outgrowth (vegetations) filled with necr. debris, thrombus and
organism.
- Causative agents: Viridans strep. (attacks previously damaged valves: 60%),
S. aureus (attacks healthy valves: 20%)
- Classification: acute and subacute
Acute: Previously healthy valve attacked, highly virulent organism. S.
aureus. Deadly in 1/2 of cases (even with AB Tx. and surgery). Rapid
developing fever, chills, weakness, malaise. Left side murmur in almost all.
Comp.: GN.
Subacute: Previously damaged valve attacked, low virulence factor.
Course wks-mths. Patients can recover with AB Tx. Non-specific symptoms.
Splenomegaly.
- PG: IE superimpose on healthy and damaged/abnormal valves, depends on
virulence factor and organism. IC patients at risk. Also drug users and
alcoholics.
Abnormal valves: Mitral valve prolapse, bicuspid aortic valve (norm.
3), calcific valvular stenosis.
non-IE:
- Non-bacterial thrombotic endocarditis (NBTE), Libman-sacks, Prosthetic
valves.
- NBTE: Diff. size deposits of fibrin, platelets and other comp. of blood on
valves. No inflamm. Sterile lesions (no microorg.), valve damage not a prereq. Lesions not destructive. Causes: endocardial trauma, hypercoagulable
states.
- Libman-sacks E.: Sterile vegetations ass. w/ SLE. Immune comp. is base of
lesions, ass. w/ inflamm. Tx: steroids.
- Prosthetic valves: Mechanical and bioprosthetic.
Mech.: Good durab., but req. constant anticoag. meds. (too much anticoag -> hemmorhage, too little -> thrombosis). RBC hemolysis due to sheer
stress.
Biopros.: From pigs or cows (or humans). No anti-coag. needed. Less
durable, may stiffen and cause stenosis, may calcify. May tear, cause insuff.
Both can be subject of infection.

91, Myocarditis. Cardiomyopathies.

Myocarditis:
- Inflamm. of myocard.
- May be caused by virus (most common), bacteria, funghi, protozoa. But also
non-infect. cases: SLE, polymyositis.
- Damage caused by direct damage, cross react AB, T-cell immune reaction
against infected cells (like hepatitis)
- Morph: ventricles most often affected. Can have mural thrombi. Inflamm.
infiltrate, foci of necr.
Lymphocytic MC: Most common, lesion heal by scarring
Hypersensitvity MC: Eosinophils
Giant cell MC: Inflitrate of multinucleated cells, more aggressive
Chagas MC: due to T. cruzi.
- CF: some asymptomatic w/ complete recovery. Can lead to HF, arrhythmias
(SCD). Fatigue, dyspnea, palp., pain, fever. Develop dilated cardiomyopathy
(next)
Cardiomyopathy:
Def.: Chronic disease of heart muscle. 1ry when just heart aff., 2ndry when
part of generalised organ disorder.
- Class.: Dilated, hypertrophic, restrictive
Dilated CM: Progress. dilation, followed by cardiac dysfunction.
Causes: viral, alcohol and other toxins, genetic, peripartum.
Morph: heart 3x size, flabby, dilated, wall thickness range from thinner to
thicker than norm., mural thrombi, valvular insuff., myocytes are
hypertrophied.
CF: 20-50s mostly. Slow progressing CHF. Heart transplant needed in the end.
Hypertrophic CM: Myocardial hypertrophy, ab. dias. filling, ventricular
outflow obs. Heart is thick and heavy. Systolic function is preserved.
Morph: myocardial hypertrophy w/o dilation. LV cavity is banana shaped.
Interstitial fibrosis b/w myocytes.
CF: Big heart, small SV. Impaired diastolic filling due to small chamber.
Poor blood flow to coronaries, myocardial ischemia, angina.
Restrictive CM: Stiff heart with poor compliance. Systolic function is
preserved, impaired diastolic filling, interstitial fibrosis.
2 types: Endomyocardial fibrosis - MCC of RCM, heavy fibrosis in heart;
Loeffler endomyocarditis - endocard. fibrosis.