Week 5 (Diseases of Cardiovascular Structures) Flashcards
Areas of auscultation for each valve
APTM: all physicians take money
Aortic valve: 2nd right intercostal space
Pulmonic valve: 2nd left intercostal space
Tricuspid valve: lower left sternal border
Mitral valve: apex
Two methods to calculate valve flow rate and area
1) Cardiac catheterization: divide CO by period of time that the valve is open (diastolic filling time for mitral and systolic ejection time for aortic valve)
2) Doppler echocardiography: uses high frequency ultrasound to evaluate cardiac structures and hemodynamics
What happens to systole and diastole when HR increases?
Length of systole shortens somewhat with increasing HR
Diastolic filling time and each diastolic filling period is shortened with increasing HR
Increasing HR without any increase in CO markedly increases mitral valve flow (and makes mitral stenosis worse)
Valve lesions that cause pressure vs. volume overload
Pressure overload caused when valve lesion causes obstruction to ventricular outflow which causes hypertrophy (more than dilation) of the affected ventricle, thereby maintaining a more favorable LaPlace relationship
Volume overload caused when regurgitant lesions of either inflow or outflow valves cause ventricle to dilate to accommodate mandatory increase in SV (and develop hypertrophy to a lesser extent)
Mitral stenosis
Causes: recurrent attacks of acute rheumatic fever resulting in rheumatic heart disease (common), congenital (parachute mitral valve, supravalvar mitral ring), systemic disease (carcinoid, SLE, rheumatoid arthritis, mucopolysaccharidosis, healed endocarditis)
Specific to rheumatic: mitral orifice restricted by commissural fusion, scarring and/or calcification of leaflets, variable degrees of subvalvar pathology (thickening and shortening of chordae and elongation of papillary muscles); stenosed valve may become tapered like a funnel or rendered into “fish mouth”
Afib is common and results from dilation of atrium from elevated pressure and inflammation and scarring of atrial walls from rheumatic process
Stagnation of blood in atrium often results in thrombus formation and may cause systemic embolism
Is considered severe if mitral valve area <1cm2, resting mean pressure gradient >10, PHT > 220ms
Auscultation findings in mitral stenosis
Loud S1: elevated LA pressure, mitral valve closes later and more loudly than normal; JVP is a-wave dominant and a-wave occurs with loud S1
Opening snap: happens early diastole; mitral valve opens earlier than normal (LA pressure), fused leaflets abruptly halt mitral valve opening (like sail hitting the wind hard) in diastole causing OS
Mid-diastolic murmur: corresponds with high LA-LV gradient
Presystolic murmur: at very end of diastole when you have atrial kick, get increased volume because increased flow
Hear murmurs better at apex; hear OS better at base/aortic region
Complications with mitral stenosis
Afib is very common
Embolic events are common
Serious and feared complication is pulmonary hemorrhage resulting from rupture of high pressure bronchial veins (which drain into LA)
Should be considered in differential for any pt presenting with hemoptysis
Pregnancy often provokes symptoms in previously asymptomatic subjects with mitral stenosis because of added burden of increased blood vol and CO (in pregnant woman with sx, use beta blockers or diuretics)
Therapies for mitral stenosis
1) Control HR to increase diastolic filling time, decrease LA pressure and decrease pulm capillary bed pressure to prevent pulmonary edema; use digoxin, beta blockers, NOT arterial vasodilators (nitrates) or ACEI because lower SVR decreases BP/cerebral perfusion pressure provoking tachycardia and decreased diastolic filling time
2) Diligent dental care with endocarditis prophylaxis (amoxicillin 2g one hr before procedure)
3) Prevention and conversion of afib: antiarrhythmatics to maintain sinus rhythm (amiodarone); electrical or chemical cardioversion (after anticoagulation or TEE); all pts should be chronically anticoagulated with warfarin with target INR 2
4) Percutaneous balloon valvuloplasty is widely used; contraindicated if more than mild regurg or LA thrombus; have to go in thru RA, create small PFO getting to LA but that’s okay because helps decompress LA!
5) Surgical treatment if patient not candidate for balloon valvuloplasty (open mitral valvotomy if mild, mitral valve repair, or mitral valve replacement)
Mitral regurgitation
Causes: leaflet abnormalities (myxomatous degen of leaflets, rheumatic disease, endocarditis), congenital, annular abnormalities, chordal abnormalities (rupture resulting in flail leaflet, rheumatic), papillary muscle abnormalities (rupture, ischemia, amyloid, sarcoid)
Chronic mitral regurg well tolerated since heart can compensate for volume overload with increased compliance and increased SV
Symptoms of fatigue due to low CO late in disease when heart markedly enlarged or when afterload increases because of HTN or peripheral vascular changes of aging
Eventually, something can tip the pt over and compensatory mechanisms fail, heart dilates, HTN downstream causes more mitral regurg, can develop atrial arrhythmia
Acute mitral regurg may subject the left heart chambers to a smaller volume overload than chronic regurg, but LV diastolic pressure and LA pressure during ventricular systole increases so considerable back pressure on pulmonary veins and resultant dyspnea
Forward CO may be compromised by inability of L heart chambers to accommodate sufficient volume to maintain normal forward SV in face of back leakage
Findings in mitral regurg
Inspection: apex beat displaced to 7th L intercostal space, outward excursion of stethoscope head during systole
Auscultation: blowing murmur; thudding sound with inward return of stethescope; heart murmur is holosystolic best heard over apex and radiates toward axilla; loud S1 initiates explosive systolic murmur and barely hear the S1 and S2; if failing ventricle, have S3 at apex and means poor prognosis
If ruptured cord, have early systolic murmur that is not holosystolic because of pressure gradients (means LA pressure really high)
Mitral valve prolapse
Volume of regurgitant flow is usually small, but some patients may develop progressively severe regurg or rupture of chordae
Causes: myxomatous degeneration, rheumatic fever, or chordae rupture
Symptoms frequently out of proportion to relatively mild hemodynamic impairment (chest pain and severe fatigue, palpitations/arrhythmias)
Most frequent valve lesion, occurs in young (skinny?) women people
Usually benign but can predispose to infective endocarditis
Sounds: late systolic crescendo (loudest at S2) heard best over apex murmur with midsystolic click (due to sudden tensing of chordae tendinae)
Murmur enhanced by maneuvers that decrease venous return (standing or valsalva), murmur may disappear if you squat down
Management of mitral regurgitation
Is a self-perpetuating processs in that ventricular, anular and atrial dilation progressively increase severity of valve incompetence
Valve repair or replacement should be performed if pt has symptoms, or asymptomatic in presence of LV dilation and decreasing systolic function, or with mitral valve prolapse with severe MR (torn chord/flail leaflet)
Medical therapy for chronic mitral regurg similar to that in patients with CHF:
1) Afterload reduction: ACEI, ARB
2) Diuretic and nitrates reduce preload and intravascular volume
3) Ventricular rate controlling agents and antiarrhythmics: beta blockers and digitalis
Aortic stenosis
Causes: most commonly bicuspid (if under 70yo), rarely unicuspid or quadracuspid; acquired “senile” calcific aortic stenosis (if over 70yo), post-inflammatory (rheumatic), combination of congenital and acquired
Stenosis of semilunar valve or ventricular outflow results in pressure overload, and elevation of ventricular pressure to overcome the obstruction
Pulsus parvus et tardus: arterial pressure pulse downstream from the obstruction rises slowly (slow carotid upstroke?); arterial pulse pressure diminished and duration of ventricular ejection lengthens (delay)
LV which is ischemic or in borderline compensation at rest is rendered increasingly ischemic with and after exercise –> exertional dyspnea due to increased filling pressure of ischemic and hypertrophic ventricle, angina, syncope, sudden death
Severe if aortic valve area <0.75 cm2 or if mean systolic gradient >50 mmHg
Findings in aortic stenosis
Auscultation: ejection click (due to abrupt halting of valve leaflets; heard at 3rd RICS?) right after S1 followed by crescendo-decrescendo midsystolic systolic ejection murmur (heard best at base/aortic area) that radiates to carotids; ends before S2
In severe AS, the LV pressure rises and increases LV-Aortic gradient and murmur will peak later
Inspection: carotid pulses delayed and diminished
Other findings: high velocity outflow on CW doppler
Natural history of aortic stenosis
Good ventricle can compensate for outflow obstruction with hypertrophy so AS may be well tolerated for years until demands of hypertrophy cause decompensation or sudden death
Once symptoms develop, risk of death from AS increases (angina gets 5 years, syncope gets 2 years and CHF gets 1 year)
Rheumatic AS (usually mitral valve involved too though) becomes symptomatic in 40s or 30 years after attack of rheumatic fever
Congenital bicuspid AS has bimodal distribution of infancy and >40yo
Senile calcific AS unlikely in patients <65
Management of aortic stenosis
Severe symptomatic AS treated surgically by aortic valve replacement or less frequently aortic valve repair (for minimally calcified bicuspid valves)
Patients <70 without contraindications or averseness to warfarin receive mechanical valve which does not require reoperation
Patients >70 or those with contraindication to warfarin of women wishing to become pregnant receive bioprosthetic (porcine or bovine pericardial) valve (but these show structural deterioration and require reoperation, no good)
Life-long endocarditis prophylaxis
Aortic regurgitation
Backflow of blood into LV results from failure of coaptation of aortic valve leaflets
Caused by valvar or aortic root disease: scarring of leaflets (congenital bicuspid, rheumatic scarring), aortic root pathology (tertiary syphilis, Marfan’s, ankylosing spondylitis, dissecting aneurysm)
Get dilation which cannot occur indefinitely, and low aortic diastolic pressure cannot provide adequate perfusion pressure for coronary arteries
LV may have to pump 10-20 L/min just to maintain NET output of 5 L/min
Resulting dilation and hypertrophy lead to massive increase in heart size
Findings in aortic regurgitation
Bounding (Corrigan’s) pulse
Head bobbing (Musset’s sign)
Auscultation: to-fro murmur that is midsystolic and early diastolic
Hear to-FRO in 3rd right intercostal space
Hear TO-fro in 2nd right intercostal space
Diastolic murmur: Austin Flint/pseudo mitral stenosis in severe AR heard at apex
If have AF, triple cadence consisting of midsystolic murmur, S2 initiating a brief early diastolic murmur, AF itself is mid-diastolic murmur superimposed on early diastolic murmur (to-fro-FRO); tachycardia; dynamic, displaced apical impulse (AF head at apex)
Chronic AR: at base hear midsystolic murmur (Ao outflow), end diastolic murmur (Ao regurg) and at apex hear Austin Flint (mitral inflow), split S1 (S1 + ejection sound)
Acute AR: at base hear midsystolic murmur (Ao outflow), end diastolic murmur abbreviated, at apex hear Austin Flint (mitral inflow) and absent S1 (ejection sound only); absence of S1 is because mitral valve flutters to near closed in middle of diastole because LV pressure so high = functional mitral stenosis; this pt is going to die
Markers of severe aortic regurgitation
Regurgitant jet width/LV outflow tract diameter ratio > 60%
Regurgitant jet area/LV outflow tract area >60%
Aortic regurgitation PHT <250
Natural history of aortic regurgitation
Compensatory mechanisms in chronic regurgitation may permit two to three decades of absent or minimal symptoms
Because of inherent limitations of these compensations, rapid deterioration occurs once decompensation sets in
Rapid decline often results from irreversible LV dilation and dysfunction
Management of aortic regurgitation
Once symptoms develop and ventricles enlarge or demonstrate decrease in systolic function, operative repair or replacement is imperative
Medical management of chronic regurgitation with afterload reducing agents (ACEI, ARB, CCB) may delay progression to poorly tolerated ventricular failure
Urgent/emergent surgery is warranted in acute severe AR
What is cholesterol required for?
Cell membranes
Precursor for other steroids: cortisol, progesterone, estrogen, testosterone, bile acids
Summary of lipoprotein functions
Chylomicron: deliver TGs (fatty acids) from dietary fat to peripheral tissue (muscle, adipose); turn into chylomicron remnants after LPL+ApoCII acts on them
Chylomicron remnants: deliver dietary cholesterol to the liver
VLDL: deliver TGs from the liver to peripheral tissue (muscle, adipose)
IDL: deliver TGs and cholesterol to liver
LDL: deliver cholesterol (derived from liver synthesis) to peripheral tisues (muscle, adipose) because tissues do receptor mediated endocytosis to take up LDL; formed after hepatic lipase (HL) modifies IDL; is this because VLDL has run out of TG to give away and is only left with mostly cholesterol?
HDL: collects (scavenges) cholesterol from peripheral tissues and delivers it back to liver (mediates reverse cholesterol transport!); acts as repository for ApoC and ApoE (which are needed for chylomicron and VLDL metabolism)
LDL, HDL, and TGs (the lipids)
LDL: lousy cholesterol; major cholesterol carrier in the blood; excess most likely leads to atherosclerosis; pro-inflammatory?
HDL: healthy cholesterol; transports cholesterol away from arteries and back to liver (via ABC-1 transporter, and mature HDL taken up by liver via hepatic scavenger receptor class B) to be eliminated; antioxidant and anti-inflammatory properties
Triglycerides: chemical form in which most fat exists in foods; made in the body from other energy sources like carbs; calories ingested in meal that are not immediately used by tissues are converted to TGs; hormones regulate release from fat tissue to meet body’s needs for energy between meals
Type I Familial Hyperchylomicronemia
High chylomicrons, high TG, high cholesterol
Creamy plasma
AR, deficient in lipoprotein lipase or altered ApoCII (rare)
Causes pancreatitis (this can kill kids), hepatosplenomegaly, eruptive/pruritic xanthomas (no increased risk for atherosclerosis)
Treatment is low fat diet (no drug therapy)
Type IIa Familial Hypercholesterolemia
High LDL, high cholesterol
Clear plasma
AD, absent or decreased LDL receptors
Causes accelerated atherosclerosis, tendon (Achilles) xanthomas, corneal arcus
Treatment is low cholesterol and low saturated fat in diet; drug therapy to lower LDL
Type IIb Familial Combined Hyperlipidemia
Similar to IIa but VLDL also increased, in addition to TGs and cholesterol
Plasma often turbid
Caused by overproduction of VLDL by the liver
Treatment is dietary restriction of cholesterol, saturated fat and alcohol; Drug therapy (maybe target TGs too)
Type IV Familial Hypertriglyceridemia
High VLDL, TGs
Plasma turbid
AD, hepatic overproduction of VLDL or decreased removal of VLDL TG
Causes pancreatitis
Treatment is weight reduction, dietary restriction of carbs, modified fat, low alcohol consumption; drug therapy
More common now because associated with diabetes
Exogenous vs. endogenous pathways of cholesterol metabolism
Exogenous (dietary) lipid pathway: TG and cholesterol packaged into chylomicrons in epithelial cells of intestines –> chylomicrons circulate in lymph then get into blood –> LPL located on luminal surface of capillary endothelial cells releases FFA from TGs from chylomicrons to go into adipose and muscle cells –> chylomicron remnant particles removed from plasma via receptors on the liver
Endogenous lipid pathway: Liver synthesizes TG and cholesterol ester and packages them into VLDL to be released into blood –> LPL located on luminal surface of capillary endothelial cells releases FFA to be taken up by adipose and muscle cells –> some VLDL remnants are taken back up by liver via LDL receptor but remaining remnant particles become IDL –> some IDL reabsorbed by liver via LDL receptor but other IDL particles hydrolyzed by hapatic lipase (HL) to form LDL –> some LDL taken up by liver via LDL receptor but some LDL is taken up by peripheral tissue cells that have LDL receptors –> free cholesterol is released and accumulates within cells
What is the half-life for clearance of LDL?
Half-life for clearance of LDL is 24 hours
Every day about half of circulating LDL is removed via receptor mediated endocytosis
How is LDL taken up into the liver or into tissue cells?
LDL binds its receptor because ApoB100 on LDL recognizes the LDL receptor on liver or tissue cells
Once bound, entire LDL molecule is engulfed by the cell in clathrin coated pits via receptor mediated endocytosis
Endosomes turn into lysosomes and LDL is degraded
Effect of different drugs on LDL, HDL, TGs
Cholesterol absorption inhibitors (CAIs): 18% decrease LDL, 8% decrease TGs
FIbrates: 5-20% decrease LDL, 10-35% increase HDL, 20-50% decrease TGs
Niacin: 5-25% decrease LDL, 15-35% increase HDL, 20-50% decrease TGs
Resins: 15-30% decrease LDL, 3-5% increase HDL
Statins: 18-60% decrease LDL, 5-15% increase HDL, 7-30% decrease TGs
Statins
HMG-CoA Reductase inhibitors (statin is a false substrate/competitive inhibitor)
Inhibit HMG-CoA to mevalonate
Have shallow dose response curve, so initial dose is great but doubling the dose thereafter only gives 5-8% increase in efficacy
Adverse effects of statins
Pregnancy category X!!
Think liver and muscle problems because this is where cholesterol metabolized
Headache, rash, GI disturbance (dyspepsia, cramps, flatulence, constipation, abdominal pain)
Hepatotoxicity (d/c med if LFTs more than 3x upper normal limit; check LFTs at baseline, 6 wks then periodically after)
Myopathy (0.5% of patients) risk highest with lovastatin and especially in combination with fibrates
CYP3A4 drug interactions with many statins
FDA advice 2012 said new risk of T2DM and cognitive impairment (reversible within a few weeks of stopping drug), risk to liver was called rare
Red yeast rice
Fermented rice product on which red yeast has grown
RYR contains several compounds collectively known as monacolins
Monacolin K is an HMG-CoA reductase inhibitor and is the same chemical as lovastatin (same risks too)
Large variation in active compounds in RYR supplements (some supplements contaminated with citrinin, a nephrotoxic mycotoxin)–dirty preparation
Cholesterol absorption inhibitor (CAI)
Ezetimibe is the only CAI
Blocks cholesterol absorption at intestinal brush border; localize to the intestinal wall, enterohepatic circulation, minimal systemic exposure
No effect on absorption of lipid-soluble vitamins
Indications: high LDL
Pros: once daily, additive in combination with statin, limited systemic exposure, very well tolerated
Cons: some systemic exposure, 3-fold increase incidence of LFT abnormalities in combination with statins, no outcomes data
Despite LDL lowering, Ezetimibe has not been shown to decrease CV risk above what is provided by statins so seldom used in monotherapy but may be useful in combination therapy with statins
Bile acid sequestrants (resins)
Cholestyramine, colesevelam, colestipol
Bind bile acid in the intestines, interrupting enterohepatic circulation and increasing fecal excretion of the acid –> liver uses more cholesterol to make more bile acid –> decrease intrahepatic cholesterol pool –> causes some increased HMG-CoA reductase expression, increased VLDL production/secretion and LDL production, but mostly increases LDL receptors to increase LDL clearance from blood and reduce plasma LDL
Reduces LDL 20-30%
Indications: high LDL
Can be used to relieve pruritis in pts with cholestasis and/or to relieve diarrhea in post-cholecystectomy patients
Used in children because NOT systemic
Adverse effects of bile acid sequestrants (resins)
Must be taken with fluid (dispensed in powder or large tablet form)
Constipation, bloating, indigestion, nausea
Large doses may decrease absorption of fats or fat soluble vitamins
Drug interactions common (decrease drug concentration) so must take other drugs 1 hour before resin or 4 hours after
Nicotinic acid (niacin, vitamin B3)
Appears to suppress synthesis of VLDL, IDL and LDL in the liver; may increase TG catabolism and decrease HDL catabolism (in the kidney), reduces ApoB, increasees ApoA and increases HDL
Inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation (this is what FA says)
Indications: high LDL and/or high TG, combined hyperlipidemia
No additional benefit if given with statins, and also small unexplained increase in ischemic stroke with niacin
May not be used anymore since no benefit shown to pharmacologic elevation in HDL
Adverse effects of niacin
Flushing: harmless cutaneous vasodilation but very uncomfortable, can give aspirin 30 min before dose
Pruritis, rashes, dry skin
Acanthosis nigricans (velvet warty hyperpigmentation associated with insulin resistance)
Nausea and abdominal discomfort
Peptic disease
Hepatotoxicity: rare fulminant hepatic necrosis occurs with older OTC sustained release forme
Hyperuricemia in 1/5 patients that may precipitate gout
Glucose intolerance
Fibrates (fibric acid derivatives)
Gemfibrozil, clofibrate, bezafibrate, fenofibrate
Agonist of PPAR-alpha (control gene expression) to increase mitochondrial beta oxidation of FFA and decrease TG secretion and to decrease ApoCIII production (which usually inhibits TG metabolism) but increase ApoA-V production to increase TG clearance –> all lead to decreased TGs
Increase clearance of VLDL by increasing action of LPL; decrease VLDL production
Increase ApoA1 secretion and upregulate ABC-A1 to increase HDL
Indications: high TG and low HDL
Adverse effects of fibrates
Rashes
GI upset
Gallstones (upper abdominal discomfort, intolerance of fried food, bloating): increased biliary cholesterol saturation, use with caution in patients with biliary disease
Displaces warfarin from plasma albumin since drug is highly protein bound, so decrease warfarin dose to reduce myopathy?
Will increase risk of statin-induced myopathy when used together (rhabdomyolysis rarely)
CYP3A4 inducers and inhibitors
CYP3A4 inducers (cause decreased activity of statins): GCs, rifampin, phenytoin, carbamazepine
CYP3A4 inhibitors (cause increased blood levels of statins): nefazodone, fluvoxamine, ketoconazole, itraconazole, erythromycin, sertraline, grapefruit juice
Pericardium
Protective sac around the heart
Made up of visceral (inside; fine, shiny) which goes around heart then reflects back on itself to form parietal (outside) layer
Contains 5-15 mL of clear fluid
Pericardial effusion
Abnormal collection of fluid in the pericardial space
Causes: pericarditis, hemopericardium, chylopericardium
Causes of pericarditis
Idiopathic
Infectious (viral, bacterial, mycobacterial, fungal)
Autoimmune (SLE, RA, scleroderma, PAN)
Dressler’s syndrome
Neoplastic disease (breast, lung, thyroid, lymphoma/leukemia, melanoma)
Uremia
Hypothyroidism (leaky capillaries cause pericardial effusion)
Drugs (INH, procainamide, hydralazine, cyclosporine)
Are all pericardial effusions symptomatic?
No
Symptoms depend on size of effusion and rate of accumulation
Slowly accumulating effusions initially asymptomatic but eventually cause cough, hoarseness, dyspnea, dysphagia
Rapidly accumulating effusions can cause hemodynamic compromise (cardiac tamponade) with collection of as little as 100mL of fluid
Cardiac tamponade
Increase in pericardial pressure that impairs cardiac function
Think of it as diastolic dysfunction, since increased pericardial pressure is so high that the ventricles cannot fill so diminished preload and decreased stroke volume
Physiologic consequences: impaired filling of cardiac chambers, SV declines, compensatory activation of sympathetic nervous system with tachycardia and increased SVR
Often presents as shock (obstructive shock), have muffled heart sounds due to abnormal layer of fluid around heart
Beck’s triad: low BP, increased JVD, distant/muffled heart sounds
Have pulsus paradoxus
Echo findings: compression of RA and RV in diastole (because they have less muscle and easier to compress than left side), increased flow into RV with bulging of intraventricular septum into LV and decreased LV filling during inspiration, IVC distended and difficulty draining into right heart
Catheterization findings: pressure in atria and diastolic pressure in ventricles elevated and equalized in all 4 chambers, equal to elevated pericardial pressure
Treatment: volume resuscitation, vasopressors, pericardiocentesis (stick needle under xyphoid process directed toward L shoulder to drain fluid), surgical management
Acute pericarditis
Inflammation of both layers of pericardium (visceral and parietal)
Classic presentation is sharp chest pain relieved with leaning forward (keeping inflamed pericardium from rubbing against firm structures including spine behind it), pain may radiate to left trapezius ridge
Pericardial rub on exam (three components: rapid ventricular filling, atrial systole, ventricular systole) sounds like choo-choo-train; evanescent and will disappear if pericardial effusion separates inflamed visceral and parietal layers so they can’t rub against each other
EKG changes: diffuse ST segment elevation (often in all leads except aVR and V1), PR segment depression, T wave inversions, if large effusion, heart swinging back and forth in effusion can create QRS complexes that increase and decrease in size as it goes to and away from electrodes
If thought to be viral/idiopathic then treat with NSAIDs, colchicine or GCs (rarely, and increase risk of recurrence of pericarditis)–don’t need to know what virus it is because no virus-specific therapy
For patients with recurrent effusions, consider pericardial window (hole in pericardium to let it drain) that provides continuous drainage into pleural or peritoneal cavity where it will be reabsorbed
Workup for pericarditis
EKG and echo
CBC
Troponin I
BUN/creatinine
Only if you think necessary: ESR/CRP, ANA, rheumatoid factor, complement levels, thyroid function tests, PPD or quantiferon gold, HIV serology
Dressler’s syndrome
AKA postmyocardial infarction syndrome
Seen 2 weeks to several months after MI
Autoimmune mechanism resulting in fibrinous pericarditis
Low grade fever, pleuritic chest pain, pericardial friction rub (3 components, with 1 systolic and 2 diastolic) and/or pericardial effusion
Treated with NSAIDs
Constrictive pericarditis
Chronic inflammation leads to thick fibrotic or calcified pericardium
Causes: tuberculous pericarditis, viral infection, connective tissue disorders, radiation, viral pericarditis where inflammation did not completely respove
Chronic inflammatory that develops over months to years
Symptoms: abdominal pain, ascites, lower extremity swelling, dyspnea
Physical findings: Kussmaul sign (paradoxic rise in JVP with inspiration because vena cava accommodates increased fluid but heart doesn’t so fluid reflects back into jugular vein), pericardial knock heard along left sternal border due to abrupt cessation of early, rapid diastolic filling; no pulsus paradoxus because RA can’t expand to let more fluid in
Diagnostic testing: CXR for pericardial calcification, echo for thickened pericardium with reduced mobility and abnormalities of ventricular septal wall motion, CT or MRI to look at pericardial thickness, R heart cath for square root sign of diastolic ventricular pressure curve (top of square root sign is because ventricular pressure stays flat because can’t fill any more)
Myocarditis
Inflammation in myocardium
Non-viral infectious causes of myocarditis: borrelia (Lyme disease) which presents as conduction system disorder, trypanosoma cruzi (Chagas disease), trichinosis (trichinella spiralis)
Most comonly associated with viral infections: coxsackie B, adenoviruses, parvovirus B19, CMV, HIV
Symptoms/signs of viral myocarditis: early sx of acute viral infection (fevers, myalgias, fatigue), sx of heart failure several weeks later (tachycardia, hypotension, elevated JVP, S3, crackles, peripheral edema)
Labs and imaging: elevated troponin, rising viral titers, on EKG see sinus tachycardia and nonspecific ST and T wave abnormalities; pericarditis findings if patient has myopericarditis, echo to look for enlarging chamber size, MRI to look for focal changes in myocardial tissue suggesting inflammation
Treatment of viral myocarditis: antivirals and immunosuppressants are not successful, treat pts with decreased EF with beta blockade, ACEI, aldosterone antagonists and diuretics as needed
Prognosis of viral myocarditis: 1/3 patients recover fully, 1/3 stabilize on medical therapy but have permanent decrease in EF, 1/3 advance and should be considered for heart transplantation
Cardiotoxic drugs
Cocaine
Alcohol
Anthracyclines (chemotherapy): doxorubicin, danorubicin
