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Small vessel disease encompasses abnormalities affecting the microvasculature of organs such as the heart, brain, and kidneys1. When small vessel disease occurs in the heart, it is also referred to as coronary microvascular dysfunction (CMVD)2,3. While the pathophysiology and diagnosis of coronary artery disease are well-established, coronary microvascular dysfunction remains less understood4. The clinical presentation of CMVD can mimic that of coronary artery disease; a key distinguishing feature is the angina without angiographic evidence of atherosclerosis3,4.
Specifically, CMVD is characterized by a triad of pathophysiological mechanisms: structural abnormalities within the microvasculature, extravascular compressive forces that impede coronary blood flow, and dysfunctional regulation of coronary vascular tone1. These factors contribute to endothelial dysfunction, which plays a crucial role in the pathogenesis of CMVD5. Endothelial dysfunction, a critical early event in the development of CMVD, involves a multifaceted disruption of the normal homeostatic functions of the endothelium, the single-celled layer lining the inner surface of blood vessels. It is characterized by impaired nitric oxide production and increased vasoconstrictor release6.
Endothelial dysfunction is not merely a passive consequence of other cardiovascular insults but an active contributor to the pathogenesis and progression of CMVD6. Previous studies reveal that inflammation plays a significant role in CMVD and can impact vascular function, potentially leading to endothelial dysfunction6,7. Cytokines, such as interleukin 6, are markedly augmented in symptomatic patients with CMVD compared with healthy controls8. In the context of coronary microvascular dysfunction, endothelial dysfunction emerges as a pivotal factor, intricately woven into the complex mechanisms that govern microvascular health and myocardial perfusion9.
In 2020, the European Society of Cardiology (ESC) Working Group on Coronary Pathophysiology and Microcirculation categorized coronary microvascular dysfunction into five groups based on the presence or absence of obstructive coronary artery disease, the chronicity or acuity of the coronary syndrome, and the occurrence of coronary no-reflow in re-perfused acute myocardial infarction. Notably, CMVD is increasingly recognized as a primary factor in angina or heart failure following successful AMI reperfusion therapy10.
Clinically, CMVD manifests across a spectrum of cardiac conditions, including stable and acute coronary syndromes, as well as heart failure. Notably, CMVD is more prevalent and associated with higher morbidity and mortality in women compared to men1.
Studies estimate that CMVD affects approximately 3 to 4 million individuals in the United States4. Data from the WISE database indicates that 3 to 4 million Americans experience myocardial ischemia despite lacking obstructive atherosclerosis11. This population faces diminished quality of life, psychological distress, and healthcare expenditures comparable to those with obstructive CAD. Moreover, microvascular disease carries a 2.5% annual risk of major adverse cardiovascular events12. While coronary artery disease rates have declined in developed Western nations over the past three decades, India has witnessed a concerning increase. Studies of Indians globally indicate a 3-4-fold higher risk of CAD compared to white Americans13, and the exact prevalence rate of CMVD in India is still unknown.
Differentiating coronary microvascular disease from epicardial coronary artery disease based solely on clinical presentation is not feasible. Non-invasive imaging techniques, such as echocardiography and nuclear perfusion, lack the sensitivity for definitive diagnosis. The current diagnostic approach relies on a combination of factors: a normal coronary angiogram, absence of epicardial spasm during acetylcholine provocation, and a coronary flow reserve less than 2.5 during adenosine-induced hyperemia13. However, each of these criteria has limitations. A strictly binary interpretation of invasive evaluation data should be avoided, favoring a more nuanced approach14.
Pharmacological treatments for coronary microvascular dysfunction include antianginal medications like beta-blockers, calcium channel blockers, and nitrates15,16. These medications reduce myocardial oxygen demand and improve coronary blood flow. Ranolazine can reduce angina symptoms and improve exercise tolerance. Statins and ACE inhibitors may improve microvascular function and reduce cardiovascular risk by targeting endothelial dysfunction14.
Scientific inquiry into the efficacy of Ayurvedic interventions for cardiac diseases remains limited. While Ayurvedic treatments for heart disease are not as widely established as conventional approaches, they are gaining recognition as potential adjuvant therapies17. In Ayurveda, heart diseases are understood holistically, encompassing physical and psychological dimensions. Ayurvedic interventions aim to address imbalances in Doshas and promote overall well-being, but the detailed descriptions of specific heart conditions may differ from modern medical classifications18.
Given the potential for cardiac emergencies, many patients initially choose modern medicine as the primary treatment, with Ayurveda often serving as a complementary approach19,20. However, some studies suggest that Ayurveda could play a more significant role in managing heart conditions17,19,20, especially when integrated with lifestyle modifications and stress management techniques. Further rigorous research is needed to validate the efficacy and safety of specific Ayurvedic treatments for heart diseases21,22.
A randomized clinical trial involving over 70 chronic heart failure patients investigated the effects of heart failure reversal therapy (HFRT), consisting of Panchakarma therapies in conjunction with standard Chronic Heart Failure (CHF) treatment, compared to standard CHF therapy alone over 6 weeks. The study demonstrated superior outcomes in the group receiving HFRT23. Another trial evaluated HFRT in 52 CHF patients with ejection fractions between 10%-30%, also highlighting the efficacy of HFRT24. A study involving 147 patients at Madhavbaug Clinics between July and December 2018 analyzed the impact of heart failure reversal therapy on aerobic capacity. Changes in VO2 max and metabolic equivalents were assessed at 30 days post-HFRT initiation and compared to baseline. Regression analysis revealed that HFRT significantly improved both VO2 max and METs in chronic heart failure patients, suggesting enhanced aerobic capacity25. However, neither of these studies specifically addressed coronary microvascular dysfunction.
In a patient with diagnosed coronary artery disease and coronary microvascular dysfunction, alongside risk factors including female sex, advanced age, and obesity, a 14-day Panchakarma course followed by a 16-week regimen of oral Ayurvedic medication, in conjunction with conventional medical treatment, led to a noticeable reduction in associated symptoms. Given the limited research on Ayurvedic interventions for cardiac conditions, this case report offers a potentially novel perspective on managing this complex presentation. The Ayurvedic protocol employed in this case involved readily accessible, cost-effective interventions26.
Case presentation: A 59-year-old female presented to our hospital on February 27, 2024, accompanied by her husband. She reported a 10-15-day history of worsening mild to moderate body aches, left ankle pain with edema, and insomnia. Additionally, she experienced dyspnea on exertion and chest pain. The patient's ambulation was restricted to 10 steps due to leg pain. The patient's medical history was notable for a 10+ year diagnosis of Coronary Microvascular Dysfunction (CMVD), hypertension managed by a cardiologist, along with a sedentary lifestyle initiated 20-30 years prior and subsequent obesity. Menopause occurred 5-6 years prior, followed by generalized debility and increased irritability. She denied any significant history of diabetes, thyroid disorders, psychiatric conditions, trauma, allergies, or adverse obstetric events. Physical examination revealed normal vital signs. She was obese with a body weight of 86 kg and height of 160 cm (BMI-33.59). She experienced severe body aches after minimal physical activity, which significantly impaired her daily functioning.
Diagnosis, assessment, and plan: A pitting edema was seen over her left ankle joint. The pit was 5 mm deep and took 20 s to vanish (grade 2). The patient exhibited anxiety related to upcoming travel. Medical records, including prior investigations and treatments, were reviewed. Complete blood count (Hemogram), Kidney Function Test (KFT), Liver Function Test (LFT), and Blood Sugar Level (BSL) are provided in Table 1. Her 2-D color Doppler Echocardiography examination revealed Normal Left Ventricular (LV) size, normal LV systolic function (LVEF=60%), no RWMA at rest, reduced LV compliance, all cardiac valves normal, Trivial MR, no AR, Trivial TR, no significant PAH, RVSP-26 mmHg, no pericardial effusion or vegetation, no I/C mass, no coarctation. The dimensions were as follows: LV: Dd/Ds:42/27 mm, IVSd: 10 mm, LVPWd mm, LA:28 mm, AO: 30 mm (Table 2, Table 3, Figure 1). Current medical documentation indicated a diagnosis of coronary microvascular dysfunction (CMVD) with coronary artery disease. She remained hemodynamically stable without active cardiac symptoms. An Ayurvedic assessment yielded a diagnosis of Vataj Hridroga. A symptom-based Ayurvedic treatment plan was initiated in conjunction with the continuation of current medications as prescribed by the patient's cardiologist. The primary treatment goal was to alleviate the presenting symptoms without exacerbating the underlying cardiac condition. The patient expressed concerns about undertaking a long-haul flight to Australia in 15 days. Her cardiologist indicated that there is no definitive treatment for coronary microvascular dysfunction (CMVD) or its associated symptoms. The Ayurvedic treatment plan consisted of two phases: an initial 14-day Panchakarma therapeutic course administered during a 19-day inpatient admission (February 27, 2024, to March 16, 2024), followed by a 16-week course of oral Ayurvedic medications (Table 4).