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Is Coronary heart Failure with Decreased Ejection Fraction Reversible? A Case-Primarily based, Integrative Strategy? | NDNR

February 19, 2026
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S.A Decker Weiss, NMD, FASA, PLC

A fancy ischemic cardiomyopathy case exploring myocardial restoration by way of guideline-directed medical remedy, system help, metabolic optimization, and experimental regenerative adjuncts.

Brief Description

This case report examines important purposeful enchancment in a affected person with extreme coronary heart failure with diminished ejection fraction following myocardial infarction, managed with optimized guideline-directed medical remedy, cardiac resynchronization remedy, and integrative metabolic and nutraceutical help. The case highlights rising potentialities for myocardial restoration whereas emphasizing that regenerative and biologic therapies stay investigational adjuncts relatively than established requirements of care.

Introduction:

Basically, skeletal muscle heals way more shortly and fully than cardiac muscle as a result of it retains a sturdy regenerative capability that the center largely lacks.

Skeletal muscle restore begins inside hours to days after harm. For gentle to reasonable harm (e.g., pressure or contusion), purposeful restoration sometimes happens inside 2–6 weeks, whereas extra extreme tears could require 8–12 weeks or longer, relying on harm measurement, vascular provide, and rehabilitation. Importantly, regeneration can restore near-normal construction and performance when the harm setting is favorable.1,2

In distinction, cardiac muscle has minimal intrinsic regenerative capability. Following myocardial harm—most notably myocardial infarction—irreversible cardiomyocyte loss happens inside minutes, and therapeutic proceeds primarily by way of fibrotic scar formation relatively than true muscle regeneration. The inflammatory and proliferative phases happen over weeks, however the ensuing scar is everlasting and non-contractile; ventricular transforming and purposeful penalties can evolve over months to years.3,4 Thus, whereas skeletal muscle therapeutic restores tissue, cardiac “therapeutic” stabilizes the harm at the price of contractile reserve.

A further consider ischemic cardiomyopathy is mitochondrial dysfunction. In skeletal muscle, mitochondria are extremely adaptable and intently linked to regeneration. After harm, satellite tv for pc cell activation and myoblast differentiation require a metabolic shift from glycolysis to oxidative phosphorylation, accompanied by mitochondrial biogenesis and transforming. Wholesome mitochondrial dynamics (fusion, fission, mitophagy) help environment friendly ATP manufacturing, restrict reactive oxygen species (ROS), and promote profitable myofiber regeneration. When mitochondrial perform is impaired—corresponding to with getting older, diabetes, or ischemia—skeletal muscle therapeutic is slower and extra incomplete.5,6

In cardiac muscle, mitochondria occupy ~30% of cardiomyocyte quantity and are important for steady high-output ATP era. Following myocardial infarction, ischemia and reperfusion trigger profound mitochondrial harm, together with lack of membrane potential, opening of the mitochondrial permeability transition pore (mPTP), and extreme ROS era. These occasions set off cardiomyocyte demise and sharply restrict any regenerative response. Surviving cardiomyocytes should improve workload with broken mitochondrial networks, contributing to opposed ventricular transforming and development to coronary heart failure with diminished ejection fraction (HFrEF).7,8 Not like skeletal muscle, cardiomyocytes have extraordinarily restricted capability to switch misplaced cells or reset mitochondrial populations at scale.

Background:

Coronary heart failure with diminished ejection fraction (HFrEF) is a medical syndrome of coronary heart failure characterised by impaired left ventricular systolic perform, sometimes outlined as a left ventricular ejection fraction (LVEF) ≤40%, with accompanying signs/indicators of congestion or low cardiac output.9 Within the context of myocardial infarction (MI), HFrEF generally develops from ischemic cardiomyopathy: irreversible myocyte loss from infarction, adopted by opposed left ventricular transforming (dilation, wall thinning, and progressive contractile dysfunction) that may culminate in power systolic coronary heart failure.10 In america, coronary heart failure total impacts an estimated ~6.7 million adults, and HFrEF represents roughly half of coronary heart failure circumstances (with the rest largely HFpEF/HFmrEF, various by age/intercourse and comorbidity).11,12

Background Idea

That is the straightforward model of the technique to assist this affected person get well. 

  1. Hold him alive, and help optimistic myocardial transforming – implant the system (CRT-D) 
  2. Use drugs to again off the neurohormonal response to coronary heart failure. 
  3. Use diet and dietary dietary supplements to lower danger components, replenish magnesium, lower irritation and oxidative stress, help mitochondrial well being and help the administration of neurohormonal dysfunction. 
  4. Use NAD+ and sluggish launch T3 (liothyronine) for mitochondrial help. 
  5. Use MSC-derived exosomes and amniotic membrane for regeneration. 

Neurohormonal Response to Coronary heart Failure

Ischemic myocardial infarction results in lack of viable myocardium, diminished cardiac output, and elevated ventricular wall stress, activating maladaptive neurohormonal pathways that drive coronary heart failure development. Decreased renal perfusion stimulates the renin–angiotensin–aldosterone system (RAAS), selling vasoconstriction, sodium retention, and opposed ventricular transforming, whereas sympathetic nervous system overactivation will increase myocardial oxygen demand, arrhythmic danger, and myocyte apoptosis. Persistent elevation of angiotensin II, aldosterone, and catecholamines perpetuates irritation, fibrosis, and progressive systolic dysfunction.13-15 In parallel, mitochondrial dysfunction and impaired myocardial energetics are actually acknowledged as central contributors to ischemic cardiomyopathy, compounding contractile failure and limiting adaptive reserve.16

The 4 pillars of guideline-directed medical remedy (GDMT) immediately counter these processes and enhance survival. Angiotensin receptor–neprilysin inhibitors (in addition to ACE inhibitors/ARBs) suppress RAAS signaling and attenuate opposed transforming whereas enhancing natriuretic peptide exercise.17 Proof-based beta-blockers blunt sympathetic overactivation and scale back sudden cardiac demise.18 Mineralocorticoid receptor antagonists inhibit aldosterone-mediated sodium retention and myocardial fibrosis.19 Sodium–glucose cotransporter 2 (SGLT2) inhibitors additional scale back coronary heart failure hospitalizations and cardiovascular mortality, with rising proof suggesting favorable results on myocardial energetics and systemic irritation.20 Collectively, these therapies deal with the dominant neurohormonal drivers of ischemic coronary heart failure.

Adjunctive nutraceutical and botanical therapies could complement GDMT by supporting mitochondrial perform and autonomic stability. Ubiquinol (diminished coenzyme Q10), an integral part of the mitochondrial electron transport chain, has demonstrated diminished cardiovascular mortality and improved purposeful outcomes in randomized trials of power coronary heart failure.21 Magnesium, a crucial cofactor for ATP-dependent processes and myocardial electrical stability, is ceaselessly poor in coronary heart failure and put up–myocardial infarction states, with repletion related to diminished arrhythmias and improved outcomes.22 Pyrroloquinoline quinone (PQQ) has been proven in human and translational research to help mitochondrial biogenesis and redox signaling, although giant end result trials stay restricted.23 Sure cardiotonic botanicals have additionally been traditionally used to affect myocardial efficiency and neurohormonal tone. Convallaria majalis incorporates cardiac glycosides that improve contractility by way of Na⁺/Okay⁺-ATPase inhibition, whereas Leonurus cardiaca (motherwort) reveals gentle damaging chronotropic and anxiolytic results that will attenuate sympathetic overactivity. Whereas these brokers must be thought of supportive relatively than disease-modifying and require cautious medical judgment, they illustrate a complementary method concentrating on each myocardial energetics and neurohormonal stress in ischemic coronary heart failure.

Gadgets

Machine-based therapies are an integral element of therapy for chosen sufferers with coronary heart failure with diminished ejection fraction (HFrEF), significantly those that stay symptomatic regardless of optimized guideline-directed medical remedy. Implantable cardioverter-defibrillators (ICDs) scale back mortality by stopping sudden cardiac demise in sufferers with LVEF ≤35% by way of termination of malignant ventricular arrhythmias. Cardiac resynchronization remedy (CRT) improves mechanical synchrony in sufferers with diminished LVEF and extended QRS period—particularly left bundle department block—leading to reverse transforming, improved purposeful capability, diminished hospitalizations, and decrease mortality. In sufferers who should not candidates for CRT or who stay symptomatic, rising neuromodulatory and contractility-enhancing therapies present extra choices: cardiac contractility modulation (CCM) delivers nonexcitatory electrical indicators through the absolute refractory interval to reinforce myocardial contractile energy and enhance train tolerance and high quality of life, and baroreflex activation remedy (Barostim) electrically stimulates the carotid baroreceptors to revive autonomic stability by decreasing sympathetic exercise and enhancing parasympathetic tone, resulting in enhancements in purposeful standing and coronary heart failure signs.24-29

Causes for Optimism

For a lot of the creator’s profession, there was little hope for sufferers in coronary heart failure aside from lengthy shot therapies and transplants (transplants are advanced and should not a most well-liked choice). Presently the drugs are considerably improved, the gadgets are efficient and have gotten more practical because the expertise develops; pure fashions corresponding to NAD+, herbals, and orthomolecular merchandise can present a extra predictable help than ever earlier than. By including in doable regeneration, HfREF is not a hopeless analysis however relatively is changing into a course of for a sluggish restoration with a major enchancment in high quality of life. 

Affected person Info and Presenting Concern

A 64 yr outdated male introduced with a wearable cardioverter-defibrillator, or a LifeVest  which was assigned from his heart specialist and transplant surgeon because of his coronary heart failure with diminished ejection fraction. His ejection fraction was 15-20% (Regular is 55+/- 10%) (EF 15–20% + signs at relaxation, frequent decompensation → NYHA IV)

The affected person had a myocardial infarction 4 months earlier with extreme injury to the areas provided by the left anterior descending artery (LAD) and a distant coronary heart assault doubtlessly affecting the mid circumflex area. 

Diagnostic Evaluation

Echocardiography:

Section # Anatomic Section Wall Area Movement Abnormality
1 Basal Anterior Anterior Wall Hypokinesis
7 Mid Anterior Anterior Wall Akinesis
8 Mid Anteroseptal Anterior Septum Akinesis
11 Mid Inferolateral Lateral Wall Hypokinesis
12 Mid Anterolateral Lateral Wall Hypokinesis
13 Apical Anterior Apex Akinesis
14 Apical Septal Apex Akinesis
16 Apical Lateral Apex Akinesis 
17 Apical Cap Apex Akinesis

Abstract: Severely diminished left ventricular systolic perform with an estimated ejection fraction of 15–20% because of in depth akinesis of the mid-anterior, anteroseptal, and apical segments, with extra hypokinesis of the basal anterior and mid-lateral partitions.

Lab Evaluation

Pertinent findings embody: 

    • Homocysteine: 37 (optimum per the creator is beneath 10) 
    • Hgb A1c: 6.8 (optimum per creator is beneath 5.4) 
    • NT-Professional-BNP: 3987 (optimum beneath 100 per creator) 
    • TSH: 19 (excessive) and Free T3: 1.8 (low) 
    • HS-CRP: 15.6 (beneath 2.0 superb per creator) 
  • oxLDL: 82 (beneath 40 superb per creator) 

Therapeutic Intervention

Step 1: Optimize medicine

The affected person was moved from Metoprolol tartrate 25 mg twice a day to carvedilol 6.25 mg twice a day (Beta/Alpha Blocker), Sacubitril/Valsartan 24/26 mgs (ARNI) 1 cap twice a day, Empagliflozin 25 mgs (SGLT2) as soon as every day for blood sugar and cardiac transforming help, and Finerenone (MRA) 10 mgs. Labs have been monitored for BUN/Creatinine, electrolytes, and a CMP. 

Step 2. Optimize Supplementation 

    • A methylation help complement was began at 2 caps twice a day to scale back homocysteine and help wholesome ranges of neurotransmitters and glutathione ranges. 
    • A mix vitamin E and natural method was added at 1 cap twice a day to scale back oxLDL (oxidative stress). 
  • A mix natural method with Convallaria majalis, Leonurus cardiaca, Craetegus spp., Melissa officinalis – 1 cap twice a day 
  • Magnesium (Gradual Launch Know-how – Dimagnesium malate) 1 twice every day, with co-factored B’s for added methylation help 

Step 3: Mitochondrial Assist 

  • PQQ (pyrroloquinoline quinone) – 10 mgs twice a day 
  • Ubiquinol – 200 mgs 4 occasions a day 
  • NAD+ – constructing to 40 mgs Sub Q thrice per week 

T3 (Liothyronine) sluggish launch compounded (no glandular or Cytomel) 2.5 mcgs twice a day

CONTROVERSIAL: DO NOT DO THIS WITHOUT PROPER TRAINING AND MONITORING 

Step 3: 

CRT-D (Cardiac Resynchronization Remedy–Defibrillator) implanted 

Step 4: 

MSC Derived Exosomes (further mobile autos or ESV’s) 

Sufferers have been defined intimately that MSC derived exosomes (further mobile autos or ESV’s) are experimental, and that security and efficacy haven’t been evaluated and should not FDA permitted for this situation. The affected person(s) understood the dialogue and signed a type of attestation. 

MSC derived exosomes (further mobile autos or ESV’s) have been administered in two strategies. (1) A Sub Q wheel was positioned simply lateral to the LLSB (350 Billion) and allowed to soak up whereas the affected person was in a partial left lateral decubitus. The identical quantity was nebulized. Therapy repeated after 90 days 

Step 3: Amniotic Membrane

Sufferers have been defined intimately that this use of amniotic membrane is experimental, and that security and efficacy haven’t been evaluated and should not FDA permitted for this situation. The affected person(s) understood the dialogue and signed a type of attestation. 

The cardiac apex space was mapped with POCUS echocardiography then cleaned with alcohol, allowed to dry, and “scuffed” to ache tolerance with a aim of erythema to the area. A 2.5 to 2.5 sq. amniotic membrane was first connected to a 3 cm by 3 cm Mepilex kind tender silicone.

Therapy repeated after 90 days 

Step 4. Vitamin

The affected person was positioned on an anti-inflammatory weight loss program absent of trans fat and sugar. 

Medical Findings

    • Homocysteine: 37 (optimum per the creator is beneath 10) – dropped to 14 
    • Hgb A1c: 6.8 (optimum per creator is beneath 5.4) – dropped to 5.8 
    • NT-Professional-BNP: 3987 (optimum beneath 100 per creator) – dropped to 1524
    • TSH: 19 (excessive) – decreased to 7 
    • Free T3: 1.8 (low) – elevated to 2.3 
    • HS-CRP: 15.6 (beneath 2.0 superb per creator) – decreased to 9.0
  • oxLDL: 82 (beneath 40 superb per creator) – decreased to 68

F/U Echocardiography

120 days – EF% elevated to 35% 

Echo repeated at 180 days as follows: 

Section # Anatomic Section Wall Area Movement
1 Basal Anterior Anterior Wall Regular
2 Basal Anteroseptal Anterior Septum Regular
3 Basal Inferoseptal Septum Regular
4 Basal Inferior Inferior Wall Regular
5 Basal Inferolateral Lateral Wall Regular
6 Basal Anterolateral Lateral Wall Regular
7 Mid Anterior Anterior Wall Hypokinesis
8 Mid Anteroseptal Anterior Septum Hypokinesis
9 Mid Inferoseptal Septum Regular
10 Mid Inferior Inferior Wall Regular
11 Mid Inferolateral Lateral Wall Regular
12 Mid Anterolateral Lateral Wall Regular
13 Apical Anterior Apex Hypokinesis
14 Apical Septal Apex Hypokinesis
15 Apical Inferior Apex Regular
16 Apical Lateral Apex Regular
17 Apical Cap Apex Hypokinesis

Inexperienced: Enchancment in phase 

Burgundy: Section recovered 

Left ventricular systolic perform is mildly to reasonably diminished with an estimated ejection fraction of 40–45% (EF 45–50% + asymptomatic → NYHA Class I), with hypokinesis involving the mid-anterior, anteroseptal, and apical segments and in any other case regular regional wall movement.

Security and Tolerability

All forms of interventions have a wonderful historical past of security and low opposed reactions and/or intolerability. The affected person didn’t report any opposed reactions nor negative effects aside from soreness close to the implanted system. 

Security Abstract 

Throughout rising biologic and metabolic interventions for peripheral neuropathy, MSC-derived exosomes, NAD⁺, and amniotic membrane–based mostly therapies display usually favorable early security profiles however stay investigational for this indication. MSC-derived exosomes are thought of doubtlessly safer than live-cell therapies because of their acellular construction, low immunogenicity, and lack of replicative capability, with preclinical research and restricted human experiences exhibiting few severe opposed occasions; nonetheless, issues stay relating to product heterogeneity, bioactive cargo results, and restricted long-term knowledge.30-35 NAD⁺ therapies, leveraging an endogenous cofactor central to mitochondrial and mobile homeostasis, are effectively tolerated in research of oral precursors, whereas parenteral administration is especially related to transient infusion-related signs and lacks standardized dosing or FDA-approved indications.36-39 Amniotic membrane–derived biologics have a protracted medical historical past in wound care and surgical procedure with low immunogenicity and uncommon severe opposed occasions, although variability in processing strategies and restricted neurologic-specific knowledge constrain conclusions for peripheral neuropathy.40-44 Rigorous manufacturing requirements and managed human trials are wanted to additional outline security and efficacy.

Comparative Security Desk

Remedy Key Security Benefits Reported Dangers / Limitations Regulatory Standing
MSC-derived exosomes Acellular; low immunogenicity; no tumorigenicity or ectopic tissue formation reported Product heterogeneity; variable sourcing/isolation; restricted long-term human knowledge No FDA-approved indications
NAD⁺ (parenteral & oral) Endogenous molecule; good tolerability (oral); reversible opposed results Infusion-related signs; lack of standardized dosing; restricted long-term injectable knowledge No FDA-approved injectable NAD⁺
Amniotic membrane Lengthy medical use; anti-inflammatory; low immunogenicity Processing variability; restricted neurologic end result knowledge; off-label neuropathy use FDA-cleared for wound/surgical use, not neuropathy

Dialogue

Mesenchymal stem cell (MSC)–derived exosomes are being explored as a cell-free biologic for HFrEF and ischemic cardiomyopathy as a result of they’ll ship cardioprotective signaling cargo (eg, microRNAs, proteins, lipids) that will modulate irritation, scale back apoptosis, and promote angiogenesis/transforming in preclinical fashions; nonetheless, human proof stays early, heterogeneous, and largely investigational, with ongoing work targeted on manufacturing, dosing, and supply challenges (eg, IV vs intracoronary vs intramyocardial) and on clarifying sturdy medical endpoints.45-46 In parallel, NAD⁺ augmentation is being studied to handle the mitochondrial/redox dysfunction that accompanies HFrEF; in a small medical trial of steady HFrEF sufferers, the NAD⁺ precursor nicotinamide riboside considerably elevated whole-blood NAD⁺ and appeared possible/tolerable, however definitive advantages on transforming, signs, hospitalizations, or mortality stay unproven and require bigger trials (notably, the medical proof base is stronger for oral NAD⁺ precursors than for injectable NAD⁺ itself in HFrEF populations).47 

Different adjunctive biologic/metabolic methods are even much less established. Amniotic membrane–derived biomaterials (and amnion-derived cell merchandise) are being investigated primarily as bioactive scaffolds/patches that ship development components and extracellular matrix indicators, with most supporting knowledge in heart problems coming from preclinical and translational work relatively than sturdy HFrEF outcomes trials.48 Liothyronine (T3) has curiosity primarily in HFrEF sufferers with low T3 syndrome, the place thyroid hormone signaling could affect contractility, vascular tone, and mitochondrial gene expression; present efforts embody feasibility and randomized research evaluating whether or not normalizing T3 is secure and indicators purposeful profit, however routine use shouldn’t be guideline-standard and requires cautious arrhythmia/ischemia danger consideration and endocrinology/cardiology oversight.49,50 General, these approaches must be framed as experimental adjuncts to—relatively than replacements for—guideline-directed medical and system remedy in HFrEF.

Comply with-up and Outcomes

The affected person is due for follow-up echocardiogram in three extra months, however one other optimistic sign is that his lab numbers are nonetheless transferring in the precise path, with an NT-proBNP of 1246. He’s in cardiac rehabilitation, and his cardiac system reveals no indicators of arrhythmia. 

Conclusion

The creator want to be clear that this isn’t onerous science within the sense that it’s observational, and that the uncooked knowledge has not been correctly crunched by a statistician. The creator doesn’t assume {that a} correlative or a causal relationship exists, simply that what has been clinically noticed is shockingly optimistic so far. The creator assumes that the dearth of a blind, and the general promotion of the therapies could have a placebo impact. 

Dr. S.A. Decker Weiss, NMD, FASA is a board-certified naturopathic doctor specializing in integrative cardiology and longevity drugs. He’s the founding father of the Weiss Coronary heart & Longevity Clinic and serves as Government Director of International Medical. Dr. Weiss is a Fellow of the American Society of Angiology and was one of many first naturopathic physicians to finish a hospital-based cardiology rotation, serving to pioneer the combination of naturopathic and standard cardiovascular care. With greater than 20 years of medical expertise, he focuses on coronary heart failure, ischemic cardiomyopathy, lipid optimization, metabolic dysfunction, and superior preventive cardiology. Dr. Weiss lectures internationally on integrative cardiovascular therapeutics and is dedicated to bridging evidence-based pure drugs with modern cardiac science.

 

 

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