{"id":614,"date":"2026-02-28T13:30:29","date_gmt":"2026-02-28T13:30:29","guid":{"rendered":"https:\/\/heartcareforyou.in\/blog\/patent-ductus-arteriosus-definition-clinical-context-and-cardiology-overview\/"},"modified":"2026-02-28T13:30:29","modified_gmt":"2026-02-28T13:30:29","slug":"patent-ductus-arteriosus-definition-clinical-context-and-cardiology-overview","status":"publish","type":"post","link":"https:\/\/heartcareforyou.in\/blog\/patent-ductus-arteriosus-definition-clinical-context-and-cardiology-overview\/","title":{"rendered":"Patent Ductus Arteriosus: Definition, Clinical Context, and Cardiology Overview"},"content":{"rendered":"\n<h2 class=\"wp-block-heading\">Patent Ductus Arteriosus Introduction (What it is)<\/h2>\n\n\n\n<p>Patent Ductus Arteriosus is a congenital heart condition where a normal fetal blood vessel remains open after birth.<br\/>\nIt involves the ductus arteriosus, a short connection between the pulmonary artery and the aorta.<br\/>\nIt is commonly encountered in pediatrics, neonatal intensive care, and adult congenital cardiology.<br\/>\nIt is often discussed when evaluating heart murmurs, pulmonary overcirculation, or pulmonary hypertension.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\">Why Patent Ductus Arteriosus matters in cardiology (Clinical relevance)<\/h2>\n\n\n\n<p>Patent Ductus Arteriosus (PDA) matters because it changes how blood flows through the heart and lungs after birth. When the ductus arteriosus stays open, blood can shunt from the higher-pressure aorta into the pulmonary artery, increasing pulmonary blood flow. Over time, the clinical impact ranges from an incidental finding (a small PDA) to meaningful cardiopulmonary disease (a large, persistent shunt).<\/p>\n\n\n\n<p>From a cardiology education standpoint, PDA is a classic model for understanding shunt physiology, pressure gradients, and the relationship between anatomy and auscultatory findings. It also highlights how neonatal physiology differs from adult physiology: the ductus is adaptive in fetal life but can become pathologic postnatally.<\/p>\n\n\n\n<p>Clinically, PDA influences diagnostic clarity and treatment planning in several settings:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Neonatology (especially preterm infants):<\/strong> PDA can contribute to respiratory difficulty and challenges in ventilator weaning, with management that often depends on the overall clinical picture.  <\/li>\n<li><strong>Pediatrics:<\/strong> PDA is a common cause of a continuous murmur and may be discovered on routine examination or echocardiography.  <\/li>\n<li><strong>Adult congenital heart disease:<\/strong> Some patients present later with an unrepaired PDA, residual shunt after closure, or complications such as pulmonary hypertension.  <\/li>\n<li><strong>Risk stratification:<\/strong> The size of the shunt and its hemodynamic effects help clinicians anticipate risks like left-sided volume overload or progressive pulmonary vascular disease.<\/li>\n<\/ul>\n\n\n\n<h2 class=\"wp-block-heading\">Classification \/ types \/ variants<\/h2>\n\n\n\n<p>PDA is typically categorized by <strong>hemodynamic significance<\/strong>, <strong>clinical context<\/strong>, and <strong>anatomic morphology<\/strong> rather than by \u201cstages\u201d in the way many acquired diseases are staged. Common, practical ways to classify it include:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>By patient population<\/strong><\/li>\n<li><strong>Preterm PDA:<\/strong> Often influenced by immaturity of the ductal tissue and neonatal physiology; clinical decisions may be closely tied to respiratory status and other comorbidities.  <\/li>\n<li><strong>Term infant\/child PDA:<\/strong> More likely discovered due to a murmur or signs of increased pulmonary blood flow.  <\/li>\n<li>\n<p><strong>Adult PDA:<\/strong> May be small and asymptomatic, previously repaired with a residual shunt, or associated with pulmonary hypertension.<\/p>\n<\/li>\n<li>\n<p><strong>By shunt size\/hemodynamic impact (conceptual)<\/strong><\/p>\n<\/li>\n<li><strong>Small (\u201crestrictive\u201d) PDA:<\/strong> Limited shunt; may be asymptomatic with a prominent murmur.  <\/li>\n<li>\n<p><strong>Moderate to large (\u201cnon-restrictive\u201d) PDA:<\/strong> Larger shunt; more likely to cause left heart volume overload, pulmonary overcirculation, and symptoms.<\/p>\n<\/li>\n<li>\n<p><strong>By clinical presentation<\/strong><\/p>\n<\/li>\n<li><strong>\u201cSilent\u201d PDA:<\/strong> Detected incidentally on imaging without an obvious murmur.  <\/li>\n<li>\n<p><strong>Symptomatic PDA:<\/strong> Associated with symptoms or evidence of cardiac or pulmonary strain.<\/p>\n<\/li>\n<li>\n<p><strong>By ductal morphology (angiographic descriptions)<\/strong><\/p>\n<\/li>\n<li>In interventional cardiology, morphology may be described to guide device selection and procedural planning. Specific schemes exist, but the practical point is that ductal shape and size affect closure strategy and feasibility.<\/li>\n<\/ul>\n\n\n\n<p>These categories overlap, and real-world classification often depends on echocardiographic findings and the patient\u2019s overall physiology.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\">Relevant anatomy &amp; physiology<\/h2>\n\n\n\n<p>The <strong>ductus arteriosus<\/strong> is a fetal vessel connecting the <strong>proximal left pulmonary artery<\/strong> (near the pulmonary trunk) to the <strong>descending thoracic aorta<\/strong> (typically just distal to the origin of the left subclavian artery). It is part of the normal fetal circulation, allowing most right ventricular output to bypass the fluid-filled fetal lungs.<\/p>\n\n\n\n<p>Key fetal-to-neonatal transitions explain why PDA occurs:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>In fetal life:<\/strong> Pulmonary vascular resistance is high, so blood preferentially flows through the ductus from the pulmonary artery into the aorta (right-to-left at the ductal level).  <\/li>\n<li><strong>After birth:<\/strong> Lung expansion and oxygenation reduce pulmonary vascular resistance, and systemic vascular resistance rises when the placental circulation is removed. These changes favor closure of the ductus.  <\/li>\n<li><strong>Physiologic closure mechanisms:<\/strong> Increased oxygen tension and decreased circulating <strong>prostaglandins<\/strong> (especially prostaglandin E2) promote ductal constriction and eventual anatomic remodeling.<\/li>\n<\/ul>\n\n\n\n<p>When the ductus remains open, the <strong>direction and magnitude of shunting<\/strong> depend on relative pressures in the aorta and pulmonary artery, which are influenced by systemic vascular resistance, pulmonary vascular resistance, and any associated cardiac or pulmonary disease.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\">Pathophysiology or mechanism<\/h2>\n\n\n\n<p>In most postnatal settings, a PDA produces a <strong>left-to-right shunt<\/strong> from the aorta to the pulmonary artery because aortic pressure exceeds pulmonary artery pressure. The downstream effects follow basic principles of flow and volume loading:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Increased pulmonary blood flow:<\/strong> Extra blood is driven into the pulmonary circulation.  <\/li>\n<li><strong>Increased pulmonary venous return:<\/strong> More blood returns to the left atrium, increasing left atrial and left ventricular preload.  <\/li>\n<li><strong>Left-sided volume overload:<\/strong> The left ventricle may dilate over time to handle the increased volume, and patients can develop signs of congestive heart failure depending on shunt size and physiologic reserve.  <\/li>\n<li><strong>Pulmonary vascular remodeling (in some cases):<\/strong> Persistent high flow and pressure can contribute to progressive pulmonary vascular disease, raising pulmonary vascular resistance.<\/li>\n<\/ul>\n\n\n\n<p>If pulmonary vascular resistance rises substantially, the shunt may become <strong>bidirectional<\/strong> or reverse (right-to-left) at the ductus. When right-to-left flow occurs through a PDA, <strong>deoxygenated blood<\/strong> can enter the descending aorta, potentially causing <strong>differential cyanosis<\/strong> (lower extremities more cyanotic than upper extremities, because branches to the upper body arise proximal to the usual ductal insertion).<\/p>\n\n\n\n<p>In preterm infants, the physiology can be more dynamic. Ductal patency interacts with lung disease, ventilator settings, and systemic perfusion in ways that can vary by protocol and patient factors.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\">Clinical presentation or indications<\/h2>\n\n\n\n<p>Common clinical scenarios where PDA is considered include:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Continuous murmur<\/strong> noted on examination, often described as \u201cmachine-like,\u201d particularly in children with a persistent shunt.  <\/li>\n<li><strong>Bounding pulses<\/strong> or a \u201chyperdynamic\u201d precordium in more hemodynamically significant shunts.  <\/li>\n<li><strong>Signs of increased pulmonary blood flow<\/strong> such as tachypnea, feeding difficulty, or poor weight gain in infants.  <\/li>\n<li><strong>Preterm infant with respiratory instability<\/strong>, difficulty weaning respiratory support, or concern for pulmonary overcirculation (context-dependent).  <\/li>\n<li><strong>Incidental detection<\/strong> on echocardiography performed for another reason (\u201csilent\u201d PDA).  <\/li>\n<li><strong>Evaluation of pulmonary hypertension<\/strong>, where identifying shunt lesions (including PDA) is part of determining etiology and operability.  <\/li>\n<li><strong>Adult presentation<\/strong> with exertional dyspnea, a history of congenital heart disease, or a residual lesion after prior repair.<\/li>\n<\/ul>\n\n\n\n<p>Symptoms and signs vary with ductal size, pulmonary vascular resistance, and comorbid conditions.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\">Diagnostic evaluation &amp; interpretation<\/h2>\n\n\n\n<p>Diagnosis is usually confirmed with <strong>echocardiography<\/strong>, interpreted in the context of history and examination.<\/p>\n\n\n\n<p>Typical evaluation includes:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>History<\/strong><\/li>\n<li>Symptoms of pulmonary overcirculation (breathlessness, feeding intolerance in infants, exercise intolerance in older patients).  <\/li>\n<li>Growth patterns in children.  <\/li>\n<li>Prior neonatal history (prematurity, respiratory distress).  <\/li>\n<li>\n<p>Adult history of congenital heart disease repairs or unexplained murmurs.<\/p>\n<\/li>\n<li>\n<p><strong>Physical examination<\/strong><\/p>\n<\/li>\n<li><strong>Auscultation:<\/strong> Continuous murmur; in some cases, the murmur may be softer or absent (very small PDA or severe pulmonary hypertension with reduced shunt gradient).  <\/li>\n<li><strong>Pulse quality:<\/strong> Bounding pulses may suggest a significant runoff lesion.  <\/li>\n<li>\n<p><strong>Signs of heart failure:<\/strong> Tachycardia, hepatomegaly, respiratory distress, or poor perfusion, depending on age and physiology.<\/p>\n<\/li>\n<li>\n<p><strong>Echocardiography (key test)<\/strong><\/p>\n<\/li>\n<li>Direct visualization of ductal flow with <strong>color Doppler<\/strong>.  <\/li>\n<li>Assessment of <strong>shunt direction<\/strong> (left-to-right vs bidirectional vs right-to-left).  <\/li>\n<li>Evidence of <strong>left atrial\/left ventricular dilation<\/strong> suggesting volume overload.  <\/li>\n<li>\n<p>Estimation of pulmonary pressures using Doppler findings when feasible, recognizing that estimates can be limited by imaging quality and physiology.<\/p>\n<\/li>\n<li>\n<p><strong>Electrocardiogram (ECG)<\/strong><\/p>\n<\/li>\n<li>May be normal in small PDAs.  <\/li>\n<li>\n<p>Can show signs consistent with left-sided volume loading or, in advanced cases with pulmonary hypertension, right-sided strain patterns.<\/p>\n<\/li>\n<li>\n<p><strong>Chest radiograph<\/strong><\/p>\n<\/li>\n<li>\n<p>May show increased pulmonary vascular markings and cardiomegaly in larger shunts; may be normal in small lesions.<\/p>\n<\/li>\n<li>\n<p><strong>Cardiac catheterization (selected cases)<\/strong><\/p>\n<\/li>\n<li>Considered when noninvasive data are insufficient, when pulmonary hypertension is present and operability is being assessed, or as part of planned transcatheter closure.  <\/li>\n<li>Allows direct measurement of pressures and oxygen saturations to evaluate shunt magnitude and pulmonary vascular resistance.<\/li>\n<\/ul>\n\n\n\n<p>Interpretation is not based on a single finding; clinicians synthesize ductal anatomy, shunt direction, chamber size, and the patient\u2019s symptoms and comorbidities.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\">Management overview (General approach)<\/h2>\n\n\n\n<p>Management of PDA is individualized and commonly depends on <strong>age, symptoms, shunt size, and pulmonary vascular status<\/strong>. Approaches generally fall into four categories:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Conservative \/ expectant management<\/strong><\/li>\n<li>Observation may be reasonable for small, asymptomatic PDAs or in situations where spontaneous closure is anticipated (particularly in early life).  <\/li>\n<li>\n<p>In preterm infants, conservative strategies may include careful attention to respiratory status and fluid balance as part of an overall neonatal care plan; specifics vary by protocol and patient factors.<\/p>\n<\/li>\n<li>\n<p><strong>Medical therapy (most commonly in preterm infants)<\/strong><\/p>\n<\/li>\n<li>Medications that inhibit prostaglandin synthesis (nonsteroidal anti-inflammatory drugs such as <strong>ibuprofen<\/strong> or <strong>indomethacin<\/strong>) have been used to encourage ductal closure in selected neonatal patients.  <\/li>\n<li><strong>Acetaminophen (paracetamol)<\/strong> has also been used in some settings; choice of agent can vary by clinician and case.  <\/li>\n<li>\n<p>Medical therapy requires consideration of potential adverse effects and comorbidities; monitoring practices vary by institution.<\/p>\n<\/li>\n<li>\n<p><strong>Transcatheter closure (interventional cardiology)<\/strong><\/p>\n<\/li>\n<li>Many PDAs in infants, children, and adults can be closed using catheter-delivered devices (such as coils or occluder devices), depending on ductal anatomy and patient size.  <\/li>\n<li>\n<p>This approach is often considered when there is evidence of clinically meaningful shunting, left-sided volume overload, or other indications based on the overall clinical picture.<\/p>\n<\/li>\n<li>\n<p><strong>Surgical closure<\/strong><\/p>\n<\/li>\n<li>Surgery may be used when transcatheter closure is not feasible or not available, or in specific neonatal contexts.  <\/li>\n<li>Surgical techniques include ligation or division of the ductus, with approach tailored to patient factors.<\/li>\n<\/ul>\n\n\n\n<p>A critical management concept is <strong>pulmonary hypertension assessment<\/strong>. In patients with markedly elevated pulmonary vascular resistance, closing a PDA may not be appropriate and decisions require specialized evaluation; management pathways vary by clinician and case.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\">Complications, risks, or limitations<\/h2>\n\n\n\n<p>Potential complications relate to the PDA itself and to treatment strategies. Commonly discussed risks include:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>From the PDA (untreated or persistent)<\/strong><\/li>\n<li><strong>Left heart volume overload<\/strong> with possible heart failure symptoms in larger shunts.  <\/li>\n<li><strong>Pulmonary hypertension<\/strong> and progressive pulmonary vascular disease in long-standing significant shunts.  <\/li>\n<li><strong>Shunt reversal<\/strong> with cyanosis (including differential cyanosis) in advanced pulmonary vascular disease.  <\/li>\n<li>\n<p><strong>Infective endarteritis<\/strong> (infection involving the ductal or adjacent arterial tissue), historically associated with persistent PDA; risk assessment and prevention practices vary by guideline and patient factors.<\/p>\n<\/li>\n<li>\n<p><strong>From medical therapy (context-dependent, especially in preterm infants)<\/strong><\/p>\n<\/li>\n<li>Renal perfusion effects, gastrointestinal complications, and effects on platelet function or bleeding risk are commonly considered with nonsteroidal anti-inflammatory drugs.  <\/li>\n<li>\n<p>Treatment choice may be limited by comorbidities and overall neonatal status.<\/p>\n<\/li>\n<li>\n<p><strong>From transcatheter closure<\/strong><\/p>\n<\/li>\n<li>Residual shunt, device embolization or malposition, vascular access complications, and hemolysis (typically related to residual high-velocity jets) are recognized risks.  <\/li>\n<li>\n<p>In small infants, procedural feasibility and risk depend on size and anatomy.<\/p>\n<\/li>\n<li>\n<p><strong>From surgical closure<\/strong><\/p>\n<\/li>\n<li>Risks include bleeding, infection, pneumothorax, and injury to nearby structures (for example, the recurrent laryngeal nerve), with frequency influenced by patient size and clinical context.<\/li>\n<\/ul>\n\n\n\n<p>Limitations are often physiologic: when pulmonary vascular disease is advanced, closure decisions require careful assessment because the PDA may function as a \u201cpressure relief\u201d pathway in certain hemodynamic states.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\">Prognosis &amp; follow-up considerations<\/h2>\n\n\n\n<p>Prognosis for PDA is strongly influenced by <strong>ductal size, duration of shunting, pulmonary vascular response, and timing of closure (when indicated)<\/strong>. Many patients do well when a hemodynamically significant PDA is identified and appropriately managed, and smaller PDAs may have minimal lifetime impact.<\/p>\n\n\n\n<p>Key factors that shape outcomes and follow-up needs include:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Hemodynamic significance:<\/strong> Evidence of left-sided volume overload or symptoms generally implies greater clinical relevance and may prompt closer follow-up.  <\/li>\n<li><strong>Pulmonary hypertension:<\/strong> Presence and severity of pulmonary hypertension can complicate decision-making and may require specialized longitudinal care.  <\/li>\n<li><strong>Age at diagnosis:<\/strong> Long-standing unrepaired shunts may carry higher risk of pulmonary vascular remodeling, whereas earlier identification can prevent chronic consequences in selected cases.  <\/li>\n<li><strong>Post-closure follow-up:<\/strong> After device or surgical closure, follow-up commonly focuses on confirming closure, monitoring for residual shunt, and assessing heart size and function over time. The exact schedule varies by clinician and case.  <\/li>\n<li><strong>Associated conditions:<\/strong> Prematurity, chronic lung disease, or other congenital heart lesions can influence recovery trajectory and long-term monitoring.<\/li>\n<\/ul>\n\n\n\n<p>This is an area where practice varies by protocol and patient factors, particularly in preterm infants and in patients with pulmonary hypertension.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\">Patent Ductus Arteriosus Common questions (FAQ)<\/h2>\n\n\n\n<p><strong>Q: What does Patent Ductus Arteriosus mean in plain language?<\/strong><br\/>\nIt means a normal fetal connection between the aorta and pulmonary artery did not close after birth. Instead of sealing off, the vessel remains \u201cpatent,\u201d or open. This can allow extra blood to flow into the lungs.<\/p>\n\n\n\n<p><strong>Q: Is Patent Ductus Arteriosus a congenital heart defect?<\/strong><br\/>\nYes. It is a congenital heart condition because it involves a structure present from fetal development that persists after birth. It may occur alone or alongside other congenital heart findings.<\/p>\n\n\n\n<p><strong>Q: Why can Patent Ductus Arteriosus cause a continuous murmur?<\/strong><br\/>\nIn many cases, the aorta maintains higher pressure than the pulmonary artery during both systole and diastole. That sustained pressure difference can drive continuous flow through the ductus, which produces a murmur heard across the cardiac cycle. The murmur may be less obvious if the PDA is very small or if pulmonary pressures are high.<\/p>\n\n\n\n<p><strong>Q: How is Patent Ductus Arteriosus usually diagnosed?<\/strong><br\/>\nEchocardiography is the most common confirmatory test because it can visualize the ductus and measure flow with Doppler. Clinicians also use the history and physical exam to assess symptoms and hemodynamic impact. Additional tests like electrocardiogram or chest radiograph may support the overall assessment.<\/p>\n\n\n\n<p><strong>Q: What does it mean if a PDA is described as \u201chemodynamically significant\u201d?<\/strong><br\/>\nIt means the shunt is large enough to affect circulation in a clinically meaningful way. This often refers to increased pulmonary blood flow and measurable effects on the left side of the heart, such as left atrial or left ventricular enlargement. The exact definition can vary by clinician and case.<\/p>\n\n\n\n<p><strong>Q: Do all PDAs need to be closed?<\/strong><br\/>\nNot necessarily. Some PDAs are small and cause little to no physiologic burden, while others can lead to symptoms or long-term complications. Decisions about closure depend on anatomy, shunt impact, symptoms, and pulmonary vascular status, and vary by clinician and patient factors.<\/p>\n\n\n\n<p><strong>Q: How is Patent Ductus Arteriosus treated in general?<\/strong><br\/>\nManagement can include observation, medical therapy (most often in preterm infants), transcatheter device closure, or surgical closure. The approach is chosen based on patient age, duct anatomy, symptoms, and associated conditions. In patients with pulmonary hypertension, evaluation may be more complex and individualized.<\/p>\n\n\n\n<p><strong>Q: Can adults have Patent Ductus Arteriosus?<\/strong><br\/>\nYes. Some adults have an unrepaired PDA that was never detected in childhood, while others have residual flow after earlier closure. Adults may be asymptomatic or may present with exercise intolerance, a murmur, or pulmonary hypertension depending on the hemodynamics.<\/p>\n\n\n\n<p><strong>Q: What are typical expectations after PDA closure?<\/strong><br\/>\nMany patients have improvement in signs related to volume overload once the shunt is eliminated. Follow-up often focuses on confirming closure and monitoring heart function and pulmonary pressures when relevant. Recovery and monitoring plans vary by procedure type and patient factors.<\/p>\n\n\n\n<p><strong>Q: Does Patent Ductus Arteriosus affect exercise or activity?<\/strong><br\/>\nImpact depends on shunt size, symptoms, and whether pulmonary hypertension or heart dysfunction is present. Some people have no limitation, while others may notice reduced exercise tolerance. Activity guidance is typically individualized in clinical practice rather than one-size-fits-all.<\/p>\n","protected":false},"excerpt":{"rendered":"<p>Patent Ductus Arteriosus is a congenital heart condition where a normal fetal blood vessel remains open after birth. It involves the ductus arteriosus, a short connection between the pulmonary artery and the aorta. It is commonly encountered in pediatrics, neonatal intensive care, and adult congenital cardiology. It is often discussed when evaluating heart murmurs, pulmonary overcirculation, or pulmonary hypertension.<\/p>\n","protected":false},"author":4,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[],"tags":[],"class_list":["post-614","post","type-post","status-publish","format-standard","hentry"],"_links":{"self":[{"href":"https:\/\/heartcareforyou.in\/blog\/wp-json\/wp\/v2\/posts\/614","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/heartcareforyou.in\/blog\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/heartcareforyou.in\/blog\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/heartcareforyou.in\/blog\/wp-json\/wp\/v2\/users\/4"}],"replies":[{"embeddable":true,"href":"https:\/\/heartcareforyou.in\/blog\/wp-json\/wp\/v2\/comments?post=614"}],"version-history":[{"count":0,"href":"https:\/\/heartcareforyou.in\/blog\/wp-json\/wp\/v2\/posts\/614\/revisions"}],"wp:attachment":[{"href":"https:\/\/heartcareforyou.in\/blog\/wp-json\/wp\/v2\/media?parent=614"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/heartcareforyou.in\/blog\/wp-json\/wp\/v2\/categories?post=614"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/heartcareforyou.in\/blog\/wp-json\/wp\/v2\/tags?post=614"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}