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docorr confirmed amyloidosis i means no definitive treatment was done gls echo was done it showed this and why would digoxin go and hide in extra cellular for no reason
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I now have everything needed for a thorough answer. Let me put it all together.
Echo Report Analysis - Mohana Valli, 45F (Confirmed Amyloidosis)
What the Echo Shows
Here are all the extracted values from the report:
| Parameter | Value | Interpretation |
|---|---|---|
| IVSd | 1.1-1.2 cm | Mildly thickened (upper limit ~1.0 cm for females) |
| LVPWd | 1.1 cm | Mildly thickened |
| LVIDd | 4.6-4.8 cm | Normal-borderline |
| EF (Teichholz) | 40% | Reduced |
| EF (Strain-derived) | 34% | Reduced |
| FS% | 19% | Reduced (normal >25%) |
| LA diameter | 4.0 cm | Dilated (normal <3.8 cm) |
| LA/Ao ratio | 1.43 | Elevated |
| AV Vmax | 0.89 m/s | Normal |
| GLS | -7.6% | Severely reduced (normal ~ -20% or more negative) |
| RWT | 0.46-0.49 | Concentric pattern |
The GLS Story - What -7.6% Means in Amyloidosis
Normal GLS is around -18% to -22%. This patient's GLS is -7.6% - that is severely impaired. More importantly, look at the segmental strain values on the bullseye plot:
- Apex: -11, -11, -11 (relatively preserved)
- Basal/Mid segments: -3, -4, -4, -7 (severely impaired)
This is the classic "apical sparing" pattern - the hallmark of cardiac amyloidosis on strain imaging. The base and mid-walls are stiff and dysfunctional because that is where amyloid fibrils deposit preferentially and earliest. The apex, having a thinner wall and less infiltration at earlier stages, retains relatively more contractility.
According to Braunwald's Heart Disease, the diagnostic criteria for apical sparing are:
- Apical / (basal + mid) strain ratio > 0.7 - this patient clearly meets this
- LVEF / GLS ratio > 4 - here: 40 / 7.6 = 5.26 - positive (above cutoff of 4), strongly suggestive of amyloid cardiomyopathy
The textbook states:
"Characteristically, patients with cardiac amyloidosis have significantly decreased global longitudinal strain despite preserved left ventricular ejection fraction. Regional deformation heterogeneity... basal segments often are hypokinetic relative to apical segments."
- Fuster & Hurst's The Heart, 15th Ed.
Note that this patient's EF is actually reduced (40-34%), meaning she is not in the "EF-preserved" stage anymore - this is already mid-to-advanced disease.
Why Digoxin Binds to Amyloid Fibrils in the Extracellular Space
This is the key pharmacological danger in amyloidosis, and your question is exactly right to ask it.
The mechanism:
Amyloid fibrils are deposited in the extracellular interstitial space of the myocardium - between the myocytes, not inside them. These fibrils are misfolded proteins (AL = immunoglobulin light chains, or ATTR = transthyretin) that aggregate into insoluble beta-pleated sheets.
Digoxin is a highly lipophilic, protein-binding cardiac glycoside. In vitro studies have confirmed that isolated AL amyloid fibrils bind digoxin with high affinity. This binding happens because:
- The beta-sheet structure of amyloid fibrils creates hydrophobic binding pockets that can trap lipophilic drug molecules like digoxin
- Digoxin "hides" in these extracellular fibril deposits - it binds to amyloid in the interstitium instead of being metabolized or excreted normally
- This creates a reservoir effect - digoxin accumulates extracellularly in the amyloid-infiltrated myocardium
The clinical consequence: When the amyloid load fluctuates (or if any therapeutic intervention reduces amyloid), the stored digoxin can be suddenly released back into the circulation - causing unpredictable digoxin toxicity at doses that would otherwise be therapeutic or sub-toxic. The patient becomes hypersensitive to digoxin.
As the Washington Manual puts it directly:
"Digoxin should be avoided in patients with AL cardiac amyloidosis because digoxin is bound extracellularly by amyloid fibrils and may cause hypersensitivity and toxicity."
And Goldman-Cecil adds:
"Patients may be hypersensitive to digoxin because of enhanced drug binding with amyloid fibrils."
Interestingly, the same binding mechanism applies to non-dihydropyridine calcium channel blockers (verapamil, diltiazem) - they also bind amyloid fibrils and are contraindicated. There's a calcium-related mechanism thought to explain this: amyloid fibrils' affinity for bone-seeking calcium tracers (like Tc-99m pyrophosphate used in diagnostic scans) suggests a calcium-binding property that also draws CCBs in.
What Drugs Are Safe vs. Avoided in Cardiac Amyloidosis
| Avoided | Reason |
|---|---|
| Digoxin (esp. AL) | Extracellular fibril binding → toxicity |
| Non-DHP CCBs (verapamil, diltiazem) | Fibril binding + negative inotropy |
| ACE inhibitors, ARBs, ARNIs | Poorly tolerated - fixed stroke volume, hypotension |
| Beta-blockers | Generally avoided (bradycardia worsens restrictive physiology) |
| Preferred | Reason |
|---|---|
| Loop diuretics + aldosterone antagonists | Euvolemia management |
| Midodrine | If orthostatic hypotension from autonomic neuropathy |
| Anticoagulation (DOACs preferred) | Very high stroke risk even in sinus rhythm |
| Amiodarone / dofetilide | For rhythm control if AF present |
| Tafamidis | For TTR amyloidosis - reduces mortality |
Summary for This Patient
This 45-year-old female with confirmed amyloidosis shows:
- GLS of -7.6% - severely impaired
- Classic apical sparing pattern on the bullseye map (apex -11 vs base -3 to -4)
- LVEF/GLS ratio 5.26 (>4 = amyloid positive)
- EF already reduced to 34-40% = mid-to-advanced stage disease
- The echo confirms what histology confirmed - this is amyloid cardiomyopathy
And digoxin is dangerous here not because it is "wrong" as a concept, but because amyloid fibrils physically sequester it extracellularly in the myocardium - it cannot be safely dosed or predicted in this setting.
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but why did cardiologist give anyway then
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Now I have everything I need. Let me give you a thorough breakdown of this entire prescription and why the cardiologist made these choices.
Breaking Down This Prescription - Why Each Drug Was Chosen
First, the clinical picture from this prescription:
- ECG: Low voltage complex + pseudoinfarct pattern + NSR (Normal Sinus Rhythm - NOT atrial fibrillation)
- BP: 90/60 mmHg sitting AND standing (no orthostatic hypotension but hypotensive at baseline)
- NT-proBNP: 3856 (massively elevated - severe HF, normal <125)
- HS Troponin: 117.6 (elevated - ongoing myocardial injury from amyloid infiltration)
- eGFR: 98 (kidneys are fine)
- Note: "May continue cancer directed therapy" - this is AL amyloidosis, she is on chemo (or targeted therapy) through oncology
This is advanced cardiac amyloidosis with HFrEF (EF 34%), NSR, hypotension, and ongoing amyloid injury.
Now, Drug by Drug
1. Digoxin 0.25mg - FIVE times a day, 5 days a week
This is not a standard digoxin dosing schedule at all. Normal digoxin is once daily. Five times a day is unusual and honestly raises a concern about whether this was a prescription writing error or a very unconventional approach.
But here is why a cardiologist might still use digoxin in amyloidosis:
The traditional teaching says avoid digoxin in amyloidosis. However, Fuster & Hurst's Heart (15th Ed.) explicitly states:
"Despite literature to the contrary, the use of digoxin, in an effort to control atrial fibrillation rate in carefully selected patients, can be very effective and does not produce excessive toxicity in cardiac amyloidosis."
And Braunwald's notes that digoxin has been "recently reconsidered if used cautiously as adjunctive management in AF rate control."
BUT - this patient is in NSR (Normal Sinus Rhythm), not AF. So the usual justification (AF rate control) does not even apply here.
In NSR with HFrEF, digoxin's other role is its weak positive inotropic effect - it increases contractility by inhibiting Na/K-ATPase on myocytes. The DIG trial showed digoxin reduces HF hospitalizations (but not mortality) in HFrEF patients in sinus rhythm. In a patient with EF of 34%, severely reduced GLS, and very low BP (90/60), the cardiologist may have reasoned that some additional inotropy is needed and that beta-blockers cannot be used (they are avoided in amyloidosis due to hypotension and restrictive physiology).
The concern remains valid though: In AL amyloidosis specifically, the fibril-binding risk is real. If this is ATTR amyloidosis, the risk is lower. The 5-days-a-week dosing looks like it may be intended to give "drug holidays" to reduce accumulation - but frankly 5 tablets in one day is also clinically odd and warrants clarification with the treating cardiologist.
2. Valentas 100 (Sacubitril 49mg + Valsartan 51mg) - twice daily
This is ARNI (Angiostensin Receptor Neprilysin Inhibitor) - the same drug class as Entresto. The textbooks say ARBs/ARNIs are "generally poorly tolerated" in advanced amyloidosis due to fixed stroke volume and hypotension. But the patient has:
- EF of 34% (HFrEF)
- Good renal function (eGFR 98)
- No orthostatic hypotension
- BP 90/60 (already low)
The cardiologist is making a risk-benefit judgment - in HFrEF, sacubitril-valsartan has the strongest mortality benefit of any drug (PARADIGM-HF trial). Starting at a low dose (100mg = the lowest dose) in a patient who is hemodynamically borderline is a calculated gamble. If she tolerates it, the benefit is real. If BP drops further, it has to come off. This choice makes pharmacological sense given the HFrEF with preserved renal function.
3. Ivabradine (Coralan) 7.5mg twice daily
Ivabradine blocks the funny (If) current in the SA node - it slows heart rate without any effect on contractility or BP. This is ideal for amyloidosis because:
- Beta-blockers (the usual HR-lowering drugs) cause hypotension and negative inotropy - both dangerous here
- Ivabradine lowers HR without dropping BP or contractility
- Indication: HFrEF with EF ≤35%, sinus rhythm, resting HR ≥70 bpm (SHIFT trial criteria)
- This patient is in NSR - perfect fit
This is actually a smart and appropriate choice for this case.
4. Dapagliflozin (Oxra) 10mg once daily
SGLT2 inhibitor - shown to reduce HF hospitalizations and cardiovascular death in HFrEF regardless of diabetes status (DAPA-HF trial). It also:
- Has mild diuretic effect (helps congestion without BP-dropping loop diuretics)
- Protects kidneys
- Neutral on BP at this dose
- No specific contraindication in amyloidosis
Very appropriate choice. SGLT2 inhibitors are now standard of care in HFrEF.
5. Vericiguat (Gantra) 10mg once daily
Soluble guanylate cyclase stimulator. Used in worsening HFrEF - patients who are still declining despite other therapies. The VICTORIA trial showed it reduced the composite endpoint of CV death + HF hospitalizations. This drug is specifically for high-risk, worsening HF patients - which this patient clearly is (NT-proBNP 3856, troponin elevated, EF 34%). Good rational addition.
6. Midodrine 5mg - SOS
Alpha-1 agonist - causes vasoconstriction, raises BP. Given SOS because the patient has baseline BP of 90/60. If she develops symptomatic hypotension (dizziness, near-syncope) particularly after the ARNI or on standing, midodrine rescues her. This was also mentioned in the previous discussion as appropriate for autonomic neuropathy-related hypotension in amyloidosis.
7. Frusemide (Lasix) 40mg - SOS for breathlessness
Loop diuretic only when needed for acute fluid overload/breathlessness. Not given daily because she is hypotensive and over-diuresis would worsen perfusion. Cautious use is correct.
8. Melatonin 3mg at night
Likely for sleep disturbance - common in amyloidosis patients due to autonomic neuropathy and high disease burden. No pharmacological interaction with amyloid.
Summary Assessment of This Prescription
| Drug | Rationale | Concern? |
|---|---|---|
| Digoxin 0.25mg x5/day, 5 days/wk | Inotropy in HFrEF-NSR | Yes - fibril binding risk in AL; dosing schedule unusual |
| Sacubitril-valsartan 100mg BD | HFrEF mortality benefit | Hypotension risk at BP 90/60 - needs close monitoring |
| Ivabradine 7.5mg BD | HR control in NSR-HFrEF | Very appropriate |
| Dapagliflozin 10mg OD | HFrEF benefit, SGLT2 | Very appropriate |
| Vericiguat 10mg OD | Worsening HFrEF | Appropriate for high-risk patient |
| Midodrine SOS | Rescue hypotension | Appropriate |
| Frusemide SOS | Acute congestion rescue | Appropriate |
| Melatonin 3mg | Sleep | No cardiac concern |
The digoxin question: The cardiologist at Apollo (Dr. Rakesh Gopal, MD DM DNB - Cardiology) is a specialist who has clearly weighed the risks. In NSR with severely depressed EF and no other inotropic options (beta-blockers avoided, dobutamine not appropriate outpatient), digoxin's weak inotropy is one of very few tools available. The 5-day-a-week schedule may be intentional to reduce cumulative exposure. However, the 5 tablets per day instruction looks like it could be a documentation error - worth confirming whether that should actually be 5 days a week, once daily rather than five tablets in a single day.
If this is AL amyloidosis specifically, that conversation with the treating cardiologist about digoxin safety is worth having at the next review (1 week, as instructed). The note to check serum ferritin and recheck electrolytes (B.Urea, Creatinine, Potassium) at review shows the cardiologist is already planning to monitor closely.
so why give digoxin if it’s still weak inotrooic
Great question - this gets to the core of clinical reasoning. Let me think through this carefully.
The honest answer is: because there is almost nothing else.
Look at what this patient has and what drugs are off the table:
What you normally use for poor contractility (EF 34%) - and why each fails here:
| Drug | Why Can't Use It |
|---|---|
| Beta-blockers (carvedilol, metoprolol) | Already hypotensive at 90/60. Beta-blockers drop BP further, cause bradycardia, worsen the already-restricted cardiac output. Avoided in amyloidosis. |
| Dobutamine / milrinone | IV inotropes - only for inpatient acute decompensation, not outpatient |
| Levosimendan | IV only, not available as oral outpatient therapy |
| ACE inhibitors | Poorly tolerated - fixed stroke volume in amyloidosis means any vasodilation = BP crash |
| Calcium channel blockers (non-DHP) | Bind amyloid fibrils, worsen conduction block - contraindicated |
So after ruling all of those out, you are left with digoxin as the only oral inotrope that can be given outpatient.
Why "weak inotropy" still matters here:
The cardiologist is not trying to normalize EF. That ship has sailed - amyloid has replaced contractile tissue with fibrils and you cannot reverse that without clearing the amyloid (which the oncology team is working on with the cancer-directed therapy). The goal is much more modest:
Can we squeeze just enough extra stroke volume to keep this patient out of hospital and functioning day to day?
With an EF of 34% and an NT-proBNP of 3856, she is in the decompensated range. Even a 5-10% improvement in stroke volume from digoxin's inotropy - weak as it is - can mean the difference between:
- Being able to walk to the bathroom vs. being breathless at rest
- Avoiding a hospital admission this week
The DIG trial (the landmark study on digoxin in HFrEF) showed digoxin does not reduce mortality but it does reduce HF hospitalizations significantly. For a 45-year-old woman with confirmed amyloidosis who is on cancer-directed therapy, staying out of hospital is a real clinical win.
The bigger picture - why this prescription makes sense as a whole:
The cardiologist has actually layered drugs cleverly to attack the problem from multiple angles:
- Vericiguat - reduces cardiac workload via NO-cGMP pathway (no BP effect)
- Dapagliflozin - reduces congestion, cardiac fibrosis, HF hospitalizations
- Ivabradine - slows heart rate to optimise filling time (more time to fill = better output per beat)
- Sacubitril-valsartan - reduces wall stress and neurohormonal activation
- Digoxin - small but additive inotropic boost on top of all the above
None of these alone is enough. Together, they represent the maximum tolerable oral therapy for someone who cannot take beta-blockers and is hypotensive. Digoxin's weakness as an inotrope is a relative problem - in a patient where every available option is limited or risky, a weak tool used carefully is still a tool.
The real clinical calculus:
The cardiologist essentially said: "The risk of digoxin toxicity in this patient - on 5-days-a-week dosing, with good renal function (eGFR 98), and close 1-week follow-up with electrolyte monitoring - is lower than the risk of doing nothing and watching her decompensate further."
That is a defensible position. Whether you agree or not depends on whether this is AL or ATTR amyloidosis - the fibril-binding risk is established primarily for AL. The answer at next review will come from watching her potassium, creatinine, and symptoms.
why can’t we make noradrenaline oral tablets then
Brilliant question - this is pure pharmacology and the answer is fascinating.
Why Noradrenaline Cannot Be an Oral Tablet
Problem 1: It Gets Destroyed in the Gut Before Absorption
Noradrenaline (norepinephrine) is a catecholamine. The gut wall and liver contain extremely high concentrations of two enzymes:
- MAO (Monoamine Oxidase) - in the gut wall itself
- COMT (Catechol-O-Methyltransferase) - in the gut wall AND liver
The moment noradrenaline hits the intestinal mucosa, these enzymes attack the catechol ring and the amine group simultaneously. It is metabolised almost completely before it even reaches the portal circulation. This is called first-pass metabolism - and for noradrenaline, it is essentially 100%. Nothing gets through.
This is why dopamine tablets also don't exist for the same reason.
Problem 2: Even If It Survived, It Would Be Unpredictable
Catecholamines need tight, second-by-second titration. In ICU, noradrenaline is run as a continuous IV infusion precisely because:
- The half-life is 2-3 minutes
- BP response is immediate and powerful
- You can increase or decrease the dose in real time based on continuous monitoring
An oral tablet with unpredictable absorption, variable gut motility, and a 2-minute half-life would be essentially impossible to dose safely. You could swing from no effect to hypertensive crisis within minutes.
Problem 3: The Wrong Mechanism Anyway for This Patient
Even if you could deliver it orally, noradrenaline is primarily an alpha-1 agonist (vasoconstriction) with some beta-1 (inotropy). The vasoconstriction would:
- Massively increase afterload on an already failing heart (EF 34%)
- The heart would have to pump against a much higher resistance
- Net cardiac output could actually fall despite higher BP
This is why in cardiogenic shock, pure vasopressors like noradrenaline are used carefully and often combined with inotropes.
What They Did Instead - The Chemical Workaround
Pharmaceutical chemists solved this problem brilliantly for related drugs:
| Problem | Solution | Example |
|---|---|---|
| Catechol ring gets destroyed by COMT | Remove the catechol, replace with something COMT cannot attack | Salbutamol (no catechol ring - survives oral dosing) |
| Amine destroyed by MAO | Add a methyl group to block MAO access | Amphetamine (alpha-methyl group blocks MAO) |
| Need oral sympathomimetic with alpha effect | Use midodrine - a prodrug converted peripherally | Midodrine - which this patient is already prescribed! |
Midodrine IS the Oral Noradrenaline Equivalent
Look at the prescription again - midodrine 5mg SOS is already there. This is exactly the solution to your question:
- Midodrine is a prodrug - it survives gut absorption because it is not a catecholamine
- After absorption, it is converted to desglymidodrine in the peripheral tissue
- Desglymidodrine is a selective alpha-1 agonist - essentially what noradrenaline does to blood vessels
- It raises BP without entering the CNS (does not cross blood-brain barrier)
- Half-life of ~3-4 hours - actually manageable as tablets
So the cardiologist has already answered your question without stating it - midodrine is sitting right there in the prescription as the oral vasopressor for when her BP drops too low.
The Broader Principle
This is actually why prodrug design exists as a field. When a drug has the right action but wrong pharmacokinetics, chemists modify the molecule just enough to survive delivery, then let the body convert it back. The drug you want cannot be given - so you give something the body will turn INTO that drug. Midodrine to noradrenaline is a textbook example of this exact strategy.
what’s inotropes actually what are they
Great foundation question. Let me build this from scratch.
What Is an Inotrope?
The word comes from Greek:
- "ino" = fibre (muscle fibre)
- "trope" = turning / changing
So an inotrope is simply anything that changes the force of muscle contraction. Specifically, cardiac muscle contraction.
- Positive inotrope = makes the heart squeeze harder
- Negative inotrope = makes the heart squeeze weaker
What Actually Makes a Heart Cell Contract?
To understand inotropes you need to understand the basic trigger first.
When an electrical signal hits a heart muscle cell (cardiomyocyte):
Electrical signal arrives
↓
Voltage-gated Ca²⁺ channels open on cell membrane
↓
Small amount of Ca²⁺ enters from outside
↓
This triggers the sarcoplasmic reticulum (SR) to
release a MASSIVE flood of Ca²⁺ inside the cell
(this is called calcium-induced calcium release)
↓
Ca²⁺ binds to troponin C on the actin filament
↓
Troponin moves, exposes the myosin binding site
↓
Myosin head grabs actin, pulls it - CONTRACTION
↓
Ca²⁺ gets pumped back into SR
↓
RELAXATION
The key message: Calcium is the trigger for contraction. More calcium inside = stronger contraction.
Every positive inotrope works by ultimately increasing intracellular calcium - either directly or indirectly.
The Three Mechanisms of Positive Inotropes
Mechanism 1: Increase cAMP → more Ca²⁺ release
cAMP (cyclic AMP) is a second messenger inside the cell. When cAMP goes up, it activates protein kinase A, which phosphorylates the calcium channels - they open more, longer, releasing more Ca²⁺.
How to raise cAMP:
| Approach | Drug | Example |
|---|---|---|
| Stimulate beta-1 receptor (makes more cAMP) | Beta-1 agonists | Dobutamine, adrenaline, noradrenaline |
| Prevent cAMP breakdown (block the enzyme that destroys it) | PDE3 inhibitors | Milrinone, amrinone |
Mechanism 2: Block Na/K-ATPase pump (digoxin's mechanism)
This is the indirect calcium route:
Digoxin blocks Na/K-ATPase pump on cell membrane
↓
Na⁺ cannot be pumped OUT of the cell
↓
Na⁺ builds up inside the cell
↓
Na⁺/Ca²⁺ exchanger (NCX) normally pumps Ca²⁺ OUT
by letting Na⁺ in - but now Na⁺ gradient is reduced
↓
NCX works less efficiently - Ca²⁺ stays inside
↓
More Ca²⁺ available → stronger contraction
This is why digoxin is a weak inotrope - it works through a roundabout indirect pathway. It does not directly open calcium channels. It just makes the cell slightly less efficient at getting rid of calcium.
Mechanism 3: Sensitise the contractile machinery to Ca²⁺
Instead of increasing calcium, you make the troponin more sensitive to whatever calcium is already there. Same amount of calcium → bigger contraction response.
- Levosimendan works this way
- Also stabilises open state of ATP-sensitive K⁺ channels in vascular smooth muscle (vasodilation - reduces cardiac workload simultaneously)
- This is clever because you get inotropy without increasing calcium overload (which can cause arrhythmias)
All Positive Inotropes at a Glance
| Drug | Mechanism | Route | Use |
|---|---|---|---|
| Digoxin | Na/K-ATPase inhibition → ↑Na⁺ → ↑Ca²⁺ | Oral / IV | Chronic HF, AF rate control |
| Dobutamine | Beta-1 agonist → ↑cAMP → ↑Ca²⁺ | IV only | Acute decompensated HF |
| Adrenaline | Alpha + Beta-1+2 agonist | IV only | Cardiac arrest, anaphylaxis |
| Noradrenaline | Alpha-1 + Beta-1 agonist | IV only | Septic shock (mainly vasopressor) |
| Milrinone | PDE3 inhibitor → ↑cAMP → ↑Ca²⁺ | IV only | Acute HF, post-cardiac surgery |
| Levosimendan | Ca²⁺ sensitiser + K⁺ channel opener | IV only | Acute decompensated HF |
| Digoxin is the ONLY one that is orally bioavailable |
Negative Inotropes (for completeness)
These reduce contractile force:
- Beta-blockers - block beta-1 receptors → less cAMP → less Ca²⁺ release
- Non-DHP calcium channel blockers (verapamil, diltiazem) - directly block Ca²⁺ entry
- Volatile anaesthetics - depress myocardial function
- Amyloid fibrils themselves act as a structural negative inotrope - they physically replace muscle with stiff protein deposits
Connecting Back to This Patient
Mohana Valli has EF of 34%. Her myocytes still exist and can still contract - they are just being strangled by amyloid deposits in the interstitium. The remaining functional myocytes need every bit of contractile force they can get.
- Cannot use dobutamine/milrinone - she is not in ICU
- Cannot use beta-1 agonists - will cause tachycardia and arrhythmia, worsen the amyloid heart
- Cannot use levosimendan - IV only, not outpatient
- Digoxin - oral, weak, but the only tool in the outpatient inotrope toolbox
That is the whole story.
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