Why Cardiovascular Regeneration Matters

Cardiovascular disease remains the world’s leading cause of death. While medications and
surgical interventions save countless lives, they rarely regenerate heart tissue that has
already been damaged by a heart attack, chronic inflammation, or structural disease. Stem cell
therapy offers a biologically targeted way to reduce inflammation, repair injured myocardium,
and even promote new blood-vessel growth (angiogenesis).

What Are Mesenchymal Stem Cells (MSCs)?

MSCs are ethically sourced cells taken from donated umbilical-cord tissue. They can
differentiate into nine different cell types—including muscle, stromal, and endothelial
cells—and secrete powerful healing messengers called exosomes.

How Stem Cells Help the Heart

• Anti-inflammatory reset – MSCs down-regulate harmful cytokines that worsen atherosclerosis and post-infarct remodeling.
• Tissue repair & regeneration – they home to injured myocardium, encouraging viable cardiomyocytes and healthier scar tissue.
• Angiogenesis support – exosomes stimulate new micro-vasculature, improving oxygen delivery to struggling heart muscle.

Clinical Evidence Snapshot

Recent randomized and meta-analysis data show meaningful improvements in left-ventricular
ejection fraction and six-minute walk distance after targeted MSC treatment in moderate-to-severe heart-failure patients.^1,2

The CRC Approach

At Cellular Regeneration Clinic we treat three major categories of heart disease—coronary
artery disease, structural heart disease, and post-infarction heart failure—using a simple outpatient
intravenous infusion of 75 to 150 million MSCs plus 3–5 billion exosomes. A second round may
be recommended 6–12 months later for advanced cases.^3,4

For multi-organ concerns (e.g. kidney or liver strain after years of cardiac medication) higher
doses of 125–150 million cells are considered to support systemic recovery.

Meet Our Medical Team

Our cardiovascular and regenerative programs are led by seasoned physicians who combine
decades of clinical experience with cutting-edge stem-cell science:

• Dr. Jorge Tagle, M.D. – Leading stem-cell and cosmetic-surgery expert; founder of Mexico’s largest cell bank (ITC) with 30+ years in aesthetic and regenerative medicine.
• Dr. Juan Manuel Dipp, M.D. – Board-certified orthopedic & spine surgeon heading CRC’s Joints Stem Cell Program; trainer of surgeons in 26 countries.
• Dr. Valerie Arango, M.D. – Regenerative and integrative-medicine physician certified by the Mexican Consensus on Stem Cells, with extensive experience in chronic-disease protocols.
• Dr. José Manuel Valdés, M.D. – Aesthetic-medicine and longevity specialist pioneering minimally invasive regenerative techniques for facial and body rejuvenation.
• Dr. Mario A. Cota Hermosillo, M.D. – Anesthesiologist focused on pain management and advanced stem-cell applications; currently pursuing a master’s in regenerative medicine.
• Dr. Miguel Magaña, M.D. – Assistant surgeon and injectables specialist versed in the latest cosmetic and regenerative protocols.

Coronary Artery Disease (CAD)

Definition & epidemiology. Coronary artery disease describes the progressive narrowing or blockage of the coronary arteries—the vessels that supply oxygen-rich blood to the heart muscle itself. It affects hundreds of millions worldwide and remains the single largest cause of mortality, accounting for roughly one in every four deaths in developed nations.

Pathophysiology. The process begins with endothelial injury triggered by factors such as hypertension, tobacco toxins, or hyperglycemia. Low-density lipoprotein (LDL) particles infiltrate the vessel wall, become oxidized, and set off a chronic inflammatory cascade. Smooth-muscle cells proliferate, calcium accumulates, and a fibrous “cap” forms over the growing atherosclerotic plaque—gradually reducing luminal diameter and coronary blood flow.

Clinical presentation. Early CAD may be entirely silent; when stenosis exceeds ~70 %, patients typically notice exertional angina (pressure-like chest pain). Acute plaque rupture can precipitate an ST-elevation myocardial infarction (STEMI) or a non-STEMI, presenting with severe chest pain, diaphoresis, and shortness of breath. Women and people with diabetes may show atypical symptoms such as fatigue or epigastric discomfort.

Conventional management. Guideline-directed therapy centers on risk-factor control—statins for dyslipidemia, ACE inhibitors or ARBs for hypertension, antiplatelet agents, and lifestyle change. Revascularization via percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) restores perfusion in advanced or unstable cases.

Regenerative-medicine perspective. At CRC, intravenous mesenchymal stem cells (MSCs) are used as an adjunct to traditional care in select patients. MSCs release exosomes rich in vascular endothelial growth factor (VEGF) and anti-inflammatory cytokines, which may help stabilize plaques, promote collateral vessel growth, and support overall myocardial metabolism—potentially improving exercise tolerance and angina frequency.

Structural Heart Disease (SHD)

Definition & scope. Structural heart disease refers to defects in the heart’s anatomy—valves, septa, chambers, or outflow tracts—whether congenital (present at birth) or acquired over time. Common examples include aortic-valve stenosis, mitral-valve prolapse, hypertrophic cardiomyopathy, and atrial-septal defects.

Hemodynamic consequences. Abnormal structure distorts normal blood-flow patterns, increasing intracardiac pressures or causing turbulent jets that damage endothelium. Long-standing hemodynamic stress can thicken chamber walls, dilate ventricles, and eventually impair systolic or diastolic function.

Symptomatology. Depending on the lesion, patients may experience exertional dyspnea, syncope, palpitations, or lower‑extremity edema. Auscultation often reveals characteristic murmurs (e.g., crescendo–decrescendo systolic murmur in aortic stenosis). Many defects, however, remain asymptomatic until late adulthood, underscoring the importance of routine echocardiographic screening in at‑risk individuals.

Standard interventions. Treatment spans medical optimization (afterload reduction, rate control) to mechanical or catheter‑based repairs such as transcatheter aortic‑valve replacement (TAVR) and percutaneous mitral‑clip placement. Surgical septal myectomy or alcohol septal ablation can relieve outflow obstruction in hypertrophic cardiomyopathy.

Role of stem‑cell therapy. While stem cells cannot “re‑engineer” valve leaflets, they can modulate the myocardial remodeling that follows chronic pressure or volume overload. CRC protocols combine MSC infusions with platelet‑rich plasma‑derived growth factors to improve diastolic compliance, reduce fibrosis around remodeled chambers, and enhance microvascular density—supporting better functional outcomes post‑repair.

Post‑Infarction Heart Failure (PI‑HF)

Definition. Post‑infarction heart failure develops when myocardial tissue lost during a heart attack is replaced by non‑contractile scar, compromising the heart’s ability to pump effectively. Depending on infarct size and location, left‑ventricular ejection fraction (LVEF) can fall below 40 %, classifying patients in HFrEF (heart failure with reduced ejection fraction).

Remodeling dynamics. After an infarct, neurohormonal systems (renin‑angiotensin‑aldosterone and sympathetic nervous system) activate to maintain perfusion. Paradoxically, chronic activation accelerates myocyte apoptosis, chamber dilation, and wall thinning—a process dubbed adverse ventricular remodeling.

Clinical burden. Symptoms include exertional breathlessness, orthopnea, peripheral edema, and fatigue. Hospital readmission rates are high, and quality of life often declines despite optimized pharmacotherapy comprising beta‑blockers, ACE inhibitors/ARNIs, mineralocorticoid‑receptor antagonists, SGLT2 inhibitors, and loop diuretics.

Device & surgical options. Cardiac‑resynchronization therapy (CRT) can improve synchrony in those with bundle‑branch block, while implantable cardioverter‑defibrillators (ICDs) reduce sudden‑death risk. Advanced cases may require left‑ventricular assist devices (LVADs) or heart transplantation.

Regenerative strategy at CRC. Intravenous or intracoronary MSCs, often delivered 4–12 weeks post‑MI, secrete paracrine factors that curb inflammation, recruit endogenous cardiac‑progenitor cells, and enhance angiogenesis in the peri‑infarct zone. Clinical trials have reported modest but meaningful rises in LVEF (≈4–8 percentage points) and improved six‑minute walk distance. CRC augments this biologic support with tailored nutritional and exercise programs to maximize ventricular recovery.