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Explore clinically focused review articles designed to help physicians refine patient selection, understand risk factors, optimise SWL protocols, and apply evidence-based decision-making in daily stone management.
Background: The patient on antiplatelet therapy presenting for extracorporeal shock wave lithotripsy (ESWL) embodies one of the most clinically consequential dilemmas in lithotripsy practice: the tension between shock wave-induced renal parenchymal hemorrhage and the potentially catastrophic thrombotic risk of antiplatelet discontinuation — particularly in patients with drug-eluting coronary stents (DES), recent acute coronary syndrome (ACS), or cerebrovascular disease. Shock waves cause renal hemorrhage through cavitation-mediated capillary disruption; in patients with pharmacologically impaired platelet function, this injury spectrum extends from subclinical subcapsular hematoma — detectable on imaging in 11–25% of patients — to clinically significant hemorrhage requiring intervention. No randomized controlled trials exist comparing continued versus withheld antiplatelet therapy during ESWL, and the available observational literature is sparse, retrospective, and non-standardized.
Objectives: This article constructs an evidence-informed, risk-stratified clinical framework for ESWL management in patients on antiplatelet therapy. It addresses the biology of shock wave-induced renal hemorrhage and platelet function, the pharmacology and washout kinetics of each antiplatelet class encountered in practice, the cardiovascular risk of antiplatelet cessation, the pivotal Regensburg systematic review re-classifying low-dose aspirin monotherapy risk, and the paradox revealed by global endourologist practice survey data. A three-tier patient classification system based on cardiovascular indication — not merely drug identity — is presented alongside a practical intraoperative and post-procedure protocol.
Methods: A structured narrative review was conducted incorporating the Regensburg systematic Medline/PubMed review of antiplatelet and anticoagulant management during SWL (Netsch et al., J Endourol 2014; PMID: 24851726), the sentinel Ruiz and Saltzman bilateral renal hemorrhage case report (J Urol 1990; PMID: 2313074), the Saltzman hematoma incidence cohort data, the Endourology Society global practice survey of approximately 2,000 members (J Urol 2017), the 2016 ACC/AHA DAPT guideline update, the ASSURE-DES randomized controlled trial (JACC 2024), and established stent thrombosis risk data from the perioperative cardiology literature. Pharmacological washout parameters for aspirin, clopidogrel, ticagrelor, and prasugrel were synthesized alongside the cardiovascular consequence data for each agent’s interruption.
Results: The Regensburg systematic review concluded that low-dose aspirin monotherapy should not be treated as an absolute contraindication to ESWL — representing a significant evolution from historical practice. The Endourology Society survey revealed a striking practice inversion: 79% of endourologists perform ureteroscopy on aspirin, yet only 18% perform ESWL on aspirin (OR 9.2; p < 0.001), an asymmetry unsupported by comparative hemorrhage evidence. The cardiovascular cost of antiplatelet cessation is well-quantified: aspirin withdrawal carries an odds ratio of 3.1 for cardiac complications peaking at day 10 (the aspirin withdrawal syndrome), while clopidogrel cessation carries an odds ratio of 14–57 for stent thrombosis in the first 18 months after DES implantation; interrupting dual antiplatelet therapy (DAPT) within 6 weeks of coronary stenting carries a cardiovascular mortality of up to 71% — dwarfing any conceivable ESWL hemorrhage mortality. The ASSURE-DES RCT found no stent thrombosis in either continuation or cessation arm in patients beyond 1 year from DES implantation, and no significant difference in major bleeding. Critically, low molecular weight heparin is not a valid bridge for antiplatelet cessation — it does not prevent platelet-driven stent thrombosis and confers bleeding risk without antiplatelet benefit, a principle explicitly codified in ACC/AHA guidelines. A delayed perinephric hematoma case (ScienceDirect 2025) — presenting one week post-ESWL in an anticoagulated patient — underscores that hemorrhagic complications can be clinically occult and temporally remote from the procedure.
Conclusions: The governing clinical question is not whether to stop antiplatelet therapy for ESWL, but what the thrombotic consequence of stopping it is for the individual patient. A three-tier risk stratification based on cardiovascular indication — Tier 1 (low-dose aspirin monotherapy in stable cardiovascular disease), Tier 2 (DAPT beyond 12 months of DES), and Tier 3 (DAPT within 6 months of DES or 3 months of ACS) — determines the management pathway. Tier 1 patients can proceed with ESWL on aspirin with protocol modifications; Tier 2 patients require mandatory cardiology consultation and guideline-based P2Y12 cessation with aspirin continuation; Tier 3 patients should have elective ESWL deferred, with ureteroscopy on maintained DAPT preferred for urgent stone treatment. Protocol modifications for all antiplatelet patients include shock rate reduction to 60/min, mandatory energy ramping, a strict session limit of ≤ 2,000 shock waves, avoidance of NSAIDs perioperatively, and routine renal ultrasound at 48–72 hours post-procedure for Tier 2 and Tier 3 patients.
The patient on antiplatelet therapy presenting for ESWL embodies one of the most clinically nuanced dilemmas in lithotripsy practice: the tension between the bleeding risk inherent in shock wave delivery to renal parenchyma, and the potentially catastrophic thrombotic risk of discontinuing antiplatelet medication — particularly in a patient with a drug-eluting coronary stent, recent acute coronary syndrome, or cerebrovascular disease. This is not a theoretical tension. It is one that every active lithotripsy unit encounters with regularity, and one for which, as the Regensburg systematic review (Journal of Endourology, 2014) frankly acknowledges, the available literature is rare, retrospective, non-standardized, and of low quality. There are no randomized controlled trials comparing continued versus withheld antiplatelet therapy specifically during ESWL — and given the low absolute incidence of clinically significant hematoma, such trials would require enormous sample sizes to detect meaningful differences.
Despite this evidentiary landscape, a workable and evidence-informed framework can be constructed from: (1) the well-characterized biology of shock wave-induced renal hemorrhage and the contribution of platelet dysfunction; (2) the specific pharmacology and washout kinetics of each antiplatelet agent; (3) the well-established cardiovascular risk of antiplatelet withdrawal, which is far better studied than the ESWL-specific bleeding literature; (4) the growing practice survey data revealing how endourologists around the world actually manage these patients; and (5) the emerging evidence — primarily from the Regensburg group — that low-dose aspirin monotherapy may be a much weaker ESWL hemorrhage risk factor than previously assumed, and that reflexive cessation of low-dose aspirin for ESWL may be causing more cardiovascular harm than the hemorrhagic risk it prevents.
This article provides a systematic examination of each antiplatelet class encountered in practice, the evidence base for its management during ESWL, and a practical risk-stratified clinical protocol built around the nature of the patient’s underlying cardiovascular indication — not merely the pharmacology of the drug.
Every ESWL procedure causes some degree of renal parenchymal injury. The mechanism is well-established from the Indiana University experimental work of Evan, McAteer, Connors, and Willis: shock waves generate cavitation bubbles that collapse asymmetrically near tissue interfaces, producing high-velocity microjets and shocklet pressures capable of rupturing glomerular and peritubular capillaries. This vascular disruption leads to extravasation of erythrocytes into the renal parenchyma and perinephric space. Macroscopic hematuria is an invariable consequence of any technically successful ESWL treatment — its absence is actually a sign of suboptimal shock wave delivery, not a protective outcome.
The spectrum of renal hemorrhage extends from: (1) microscopic hematuria (universal); (2) gross hematuria (universal, typically clearing within 24–48 hours); (3) subcapsular or perinephric hematoma detected only on imaging (present in 11–25% of patients by systematic CT or MRI imaging); and (4) symptomatic perinephric hematoma requiring intervention — angiographic embolization, surgical drainage, or in extreme cases nephrectomy — in approximately 0.28–4.1% of patients across published series.
The critical role of platelet function in this injury spectrum lies at the intersection of hemostasis and vascular trauma: when shock waves rupture renal capillaries, normal hemostasis — initiated by platelet adhesion at the site of vascular disruption — limits the extent of hemorrhage. A patient with pharmacologically impaired platelet aggregation has a reduced capacity to contain this hemorrhage, potentially allowing a minor subcapsular bleed to evolve into a clinically significant expanding hematoma. Aspirin irreversibly inhibits cyclooxygenase-1 (COX-1) in platelets for their entire lifespan (approximately 7–10 days), impairing thromboxane A2-mediated aggregation. The P2Y12 inhibitors (clopidogrel, ticagrelor, prasugrel) block ADP-mediated platelet activation through a distinct receptor pathway — clopidogrel irreversibly, ticagrelor reversibly. The combination of both (DAPT) produces additive platelet inhibition that is substantially more potent than either agent alone.
The association between aspirin use and post-ESWL hematoma was established through a combination of case reports and cohort analyses in the early 1990s. The most influential was the case report by Ruiz and Saltzman (Journal of Urology, 1990; PMID: 2313074): a patient on aspirin who developed bilateral renal hemorrhage after ESWL, ultimately requiring transfusion and prolonged hospitalization. This case — remarkable for its bilateral nature and severity — generated substantial concern and led to aspirin cessation becoming standard practice at most lithotripsy units.
A key observation from the broader cohort literature is that clopidogrel and aspirin, even when discontinued up to 2 weeks before treatment, have been linked to hematoma formation in some series (McAteer and Evan, Seminars in Nephrology, 2008; PMC2556492). This suggests that the pharmacological effect of antiplatelet agents may persist longer than their nominal washout period — potentially through residual effects on platelet function testing even after clinical recovery — or, more likely, that patients on these medications have underlying vascular disease that independently elevates their hematoma risk.
The incidence of detectable perinephric hematomas on systematic imaging was placed in quantitative context by published series: 0.66% of all ESWL patients, 2.5% of hypertensive patients, and 3.8% of poorly controlled hypertensive patients treated on the Dornier HM3 developed clinically detectable hematomas — with aspirin and non-steroidal analgesic use identified as additional risk factors alongside hypertension and diabetes (Saltzman, J Urol, 1990). The critical insight from this data is that antiplatelet use is one of several additive risk factors, not an independent categorical disqualifier — and its weight in the overall risk calculation is modified considerably by the concurrent presence or absence of hypertension, diabetes, older age, and BMI.
Understanding the specific mechanism and washout timeline of each antiplatelet agent is fundamental to rational perioperative management. The following table summarizes the clinically relevant pharmacological parameters:
| Drug | Mechanism of Action | Platelet Effect Duration | Standard Washout Before Surgery |
|---|---|---|---|
| Aspirin (Ecosprin) 75–150 mg/day | Irreversible COX-1 inhibition → ↓ TXA2 → ↓ platelet aggregation | Permanent (7–10 days = full platelet turnover) | 7–10 days for high-bleeding-risk procedures; 3–5 days for low-risk procedures |
| Clopidogrel (Plavix) 75 mg/day | Irreversible P2Y12 (ADP receptor) blockade — prodrug requiring CYP2C19 activation | Permanent for affected platelets (5–7 days for new platelet turnover) | 5–7 days (most guidelines: 5 days minimum) |
| Ticagrelor (Brilinta) 90 mg twice daily | Reversible P2Y12 blockade — direct, not a prodrug | Reversible; ~3–5 days for recovery to normal hemostasis | 3–5 days (most guidelines: 5 days minimum) |
| Prasugrel (Effient) 10 mg/day | Irreversible P2Y12 blockade — more potent than clopidogrel, prodrug | Permanent for affected platelets (7 days for new platelet turnover) | 7 days (guidelines consensus) |
| DAPT (Aspirin + any P2Y12 inhibitor) | Combined COX-1 and P2Y12 inhibition — additive platelet suppression 3.4x higher bleeding risk than ASA alone | Dual permanent (or reversible for ticagrelor) impairment | P2Y12 inhibitor per above; ASA per above or continued depending on indication |
| Low molecular weight heparin (LMWH — e.g. enoxaparin) | Factor Xa and IIa inhibition — anticoagulant, NOT antiplatelet mechanism | Dose-dependent; ~24 hours after last dose | NOT a substitute for antiplatelet agents; different mechanism; not recommended as bridge for antiplatelet cessation |
The pivotal shift in thinking about low-dose aspirin and ESWL was catalyzed by a systematic Medline/PubMed literature review from the Department of Urology, Caritas St. Josef Medical Center, University of Regensburg, Germany, published in Journal of Endourology (Netsch, Bach, Buchholz et al., 2014; PMID: 24851726). This review comprehensively searched peer-reviewed literature on anticoagulative and antiplatelet medication management during SWL and reached the following key conclusions:
The real-world picture of how endourologists manage aspirin during ESWL was captured in a survey of approximately 2,000 members of the Endourology Society conducted in September 2016 (published in Journal of Urology, 2017). Of 184 substantive responses from six continents:
The paradox revealed by this survey is striking: ureteroscopy — an endoscopic procedure requiring ureteral access, instrumentation, and laser energy delivery — is performed by 79% of endourologists on aspirin, while ESWL — a completely non-invasive procedure — is performed on aspirin by only 18%. This inversion of perceived risk is not supported by the comparative hemorrhage literature, where subcapsular hematoma rates for URS are also reported (Bai et al., Chiu et al.), and it reflects historical precedent and convention more than contemporary evidence-based practice.
The most clinically important classification to establish when managing any antiplatelet patient for ESWL is whether they are on aspirin monotherapy (low-dose, 75–150 mg/day) or on dual antiplatelet therapy (DAPT) — aspirin combined with a P2Y12 inhibitor. These are categorically different clinical scenarios with fundamentally different risk profiles, different cardiovascular indications, and different management imperatives.
Low-dose aspirin monotherapy for primary or secondary cardiovascular prevention is a relatively low-risk interruption scenario — aspirin cessation is associated with an odds ratio of 3.1 for cardiac complications (peaking at 10 days after cessation), but this primarily represents a rebound platelet hyperaggregability phenomenon and is manageable with a brief washout period of 5–7 days when clearly indicated by the clinical context. DAPT, by contrast, is prescribed for a specific and time-critical reason: prevention of stent thrombosis following coronary stenting. Clopidogrel cessation is the most significant independent predictor of stent thrombosis, with an odds ratio of 14–57 during the first 18 months after drug-eluting stent implantation. Stopping DAPT within the first 6 weeks after stenting carries a cardiovascular mortality of up to 71% in some published series — a figure that dwarfs any conceivable ESWL-induced hemorrhage mortality.
The reason DAPT is prescribed after coronary stenting is straightforward: bare metal stents are covered by smooth muscle cells within 6 weeks and by normal endothelium within 3 months. Drug-eluting stents have a profoundly slower endothelialization rate — 13% at 3 months and only 56% at 3 years — because the antiproliferative drug coating that prevents restenosis also impairs the natural healing process. Until endothelialization is complete, the metallic stent struts are exposed to flowing blood; without antiplatelet coverage, platelet aggregation on these bare metal surfaces leads to late stent thrombosis — a rare (0.6% per year after DES) but catastrophic event with a mortality of 19–45%.
The 2016 ACC/AHA guideline update on DAPT duration after PCI represents the current standard of care: for patients with stable ischemic heart disease treated with a DES, a minimum of 6 months of DAPT with clopidogrel is recommended, with just 3 months considered for those at high bleeding risk. For patients with acute coronary syndrome (ACS) treated with DES, 12 months of DAPT is the minimum recommended duration, with longer durations considered for high-ischemic-risk patients. The prior Class I recommendation requiring delay of all elective noncardiac surgery for 1 year after DES has been modified: the guideline now recommends delaying elective noncardiac surgery for at least 6 months after DES placement.
For the lithotripsy context, these timelines generate a direct clinical framework: a patient presenting with a symptomatic renal stone within 6 months of DES placement is in the highest-risk category for DAPT interruption. Elective ESWL should be deferred if clinically possible. If the stone requires treatment (obstruction, intractable pain, infection), ureteroscopy while maintaining DAPT — despite its own bleeding risks — may paradoxically be the safer choice because it offers definitive single-session treatment without requiring antiplatelet cessation, unlike ESWL which may require multiple sessions.
The most recent rigorous RCT addressing aspirin management in patients with DES undergoing noncardiac surgery was the ASSURE-DES trial (Journal of the American College of Cardiology, 2024), which randomized patients who had received a DES > 1 year previously and were undergoing elective noncardiac surgery either to continue aspirin or discontinue all antiplatelet agents 5 days before surgery. The primary outcome was a composite of death, MI, stent thrombosis, or stroke at 30 days. The result: no stent thrombosis occurred in either group. The incidence of major bleeding did not differ significantly between groups (6.5% vs 5.2%; p = 0.39), while minor bleeding was more frequent in the aspirin group (14.9% vs 10.1%; p = 0.027). The trial failed to demonstrate a significant difference in ischemic outcomes between perioperative aspirin continuation and cessation in this specific population — though the authors acknowledged that the event rates were lower than expected, limiting statistical power.
This trial, while not ESWL-specific, is relevant to the ESWL management framework: it suggests that for patients beyond 1 year from DES implantation undergoing low-to-intermediate risk procedures, the absolute ischemic risk of temporary aspirin cessation is lower than historically feared — and the absolute hemorrhagic risk of continuation is also modest. For ESWL specifically, the procedure’s non-invasive character places it firmly in the low-to-intermediate bleeding risk category.
An important and clinically under-appreciated phenomenon relevant to all antiplatelet cessation decisions is the aspirin withdrawal syndrome: a rebound prothrombotic state that follows aspirin discontinuation, characterized by increased thromboxane A2 synthesis, elevated platelet aggregation, and increased platelet-leukocyte interaction. This rebound phenomenon peaks at 8–10 days after aspirin cessation and explains the temporal clustering of cardiovascular events in the 10-day window following aspirin withdrawal. For a patient with established coronary artery disease, this physiological rebound coincides precisely with the period during which ESWL is being performed if aspirin is withheld for the standard 7-day pre-procedure period — a timing concern that has not been adequately addressed in the urological literature.
Every patient on antiplatelet therapy presenting for ESWL should be classified into one of three risk tiers before any decision about antiplatelet management is made. This classification is based on the nature of the cardiovascular indication, not merely the drug being taken.
| Risk Tier | Patient Profile | ESWL Management Principle |
|---|---|---|
| Tier 1 — Low Cardiovascular Risk | Low-dose aspirin 75–150 mg/day for primary or secondary prevention (no coronary stent, no recent ACS); stable coronary artery disease > 12 months from any revascularization; peripheral arterial disease on aspirin only; atrial fibrillation on aspirin only. | ESWL with continued low-dose aspirin is increasingly defensible based on Regensburg evidence. If institutional protocol requires cessation: withhold aspirin 5–7 days. Cardiology consultation recommended but not mandatory for primary prevention patients. Restart aspirin 24–48 hours post-ESWL. |
| Tier 2 — Intermediate Cardiovascular Risk | DAPT (ASA + P2Y12 inhibitor) > 12 months after DES implantation; DAPT for bare metal stent > 6 months; history of stroke/TIA on DAPT; peripheral arterial disease on DAPT. | Cardiology consultation mandatory before any antiplatelet decision. For ESWL: P2Y12 inhibitor withheld per guideline timeline (clopidogrel/ticagrelor 5 days; prasugrel 7 days); aspirin continued. Resume P2Y12 inhibitor 24–48 hours post-ESWL. Ureteroscopy is a reasonable alternative to avoid interruption. |
| Tier 3 — High Cardiovascular Risk | DAPT within 6 months of DES implantation; DAPT within 3 months of ACS (even without stent); DAPT within 6 weeks of any coronary intervention; recent ischaemic stroke (< 3 months) on DAPT. | ESWL is RELATIVELY CONTRAINDICATED as an elective procedure. Defer ESWL until beyond the high-risk DAPT window if clinically possible. If stone is symptomatic/obstructing: ureteroscopy on DAPT is preferred over ESWL requiring interruption. If ESWL is absolutely necessary: proceed on full DAPT with intensified hemorrhage monitoring; cardiology must be involved and document risk acceptance. |
| Parameter | Modification for Antiplatelet Patients |
|---|---|
| Shock wave rate | Reduce to 60/min — minimizes cumulative vascular trauma per session |
| Energy ramping | Mandatory stepwise escalation — begin at lowest effective energy, titrate upward. Do not start at maximum voltage. |
| Total shock waves per session | Strict limit of ≤ 2,000 shock waves per session for antiplatelet patients — lower total energy delivery reduces parenchymal injury |
| Session spacing | Minimum 14 days between sessions — allows adequate renal recovery before the next shock wave exposure |
| Maximum number of sessions | Plan for ≤ 3 sessions; if not achieving adequate fragmentation, reassess modality choice (URS offers lower parenchymal hemorrhage risk) |
| Baseline hematocrit | Document pre-procedure hematocrit. Any drop > 3 g/dL post-ESWL warrants urgent imaging evaluation. |
| Bilateral stones | Do NOT treat bilateral renal stones in the same ESWL session in antiplatelet patients — bilateral hematoma is rare but documented (Ruiz & Saltzman case) |
| Coupling | Meticulous coupling with no air pockets — reduces energy scatter, lowers peak pressures reaching perinephric tissue |
A particularly common and challenging scenario is the patient who presents acutely with a symptomatic renal or ureteric stone while on long-term low-dose aspirin for secondary cardiovascular prevention — for example, a 65-year-old with a history of myocardial infarction on 75 mg aspirin who presents with an obstructing proximal ureteric stone. The stone requires treatment; the cardiovascular indication for aspirin is established. For this patient, ureteroscopy with holmium laser lithotripsy while maintaining aspirin is supported by the current evidence and the Endourology Society survey data showing 79% of endourologists proceed with URS on aspirin. If ESWL is preferred — either because the stone is renal, the patient is obese making URS technically demanding, or patient preference — proceeding on low-dose aspirin with protocol modifications (rate reduction, limited shock waves) is a defensible position supported by the Regensburg evidence-based review.
Patients on warfarin or NOACs (apixaban, rivaroxaban, dabigatran, edoxaban) occupy a distinct category from antiplatelet patients and are addressed here briefly for completeness. Uncorrected anticoagulation is an absolute contraindication to ESWL. For warfarin patients, the INR must be corrected to ≤ 1.5 before ESWL proceeds — typically requiring 3–5 days of warfarin cessation with documented INR on the day of the procedure. For NOAC patients, the drug must be withheld for a minimum of 24–48 hours (renal-function-dependent for dabigatran; hepatic-function considerations for rivaroxaban/apixaban) before ESWL. The decision to bridge anticoagulation with LMWH during NOAC/warfarin cessation is a cardiology and hematology decision based on the underlying thromboembolic indication — it is not routinely necessary for most AF patients undergoing brief anticoagulant interruption for ESWL.
The delayed perinephric hematoma case recently reported in ScienceDirect (2025) — a 58-year-old with hypertension, diabetes, and long-term anticoagulation who developed a massive hematoma one week after ESWL — illustrates that hemorrhagic complications in anticoagulated patients can be delayed, clinically occult until symptomatic, and of substantial magnitude. This case underscores the imperative of post-procedure imaging surveillance in all anticoagulated patients rather than symptom-driven evaluation.
A frequently overlooked risk factor is the use of non-steroidal anti-inflammatory drugs (NSAIDs) as analgesics during or immediately after ESWL. NSAIDs inhibit COX-1 in a dose- and duration-dependent (but reversible, unlike aspirin) manner, impairing platelet function for 24–72 hours after each dose. Administering ibuprofen, diclofenac, or ketorolac to a patient who is already on low-dose aspirin creates a combined platelet inhibition that is clinically significant. In ESWL patients: avoid NSAIDs as analgesics for the procedure itself and for 48–72 hours post-ESWL wherever possible. Paracetamol (acetaminophen) and opioid analgesia are the preferred alternatives.
| Contraindication Type | Condition |
|---|---|
| Absolute | Uncorrected coagulopathy: INR > 1.5, platelet count < 80,000/μL — correct before proceeding |
| Absolute | Full anticoagulation (warfarin, NOAC) at therapeutic levels at time of ESWL — must be withheld and INR/drug levels confirmed before proceeding |
| Absolute | Active bleeding diathesis (haemophilia, von Willebrand disease) — correct factor deficiency before ESWL; haematology co-management required |
| Relative | DAPT within 6 months of DES implantation — defer elective ESWL; prefer URS if treatment urgent |
| Relative | DAPT within 3 months of ACS — defer ESWL; cardiology mandatory before any antiplatelet decision |
| Relative | Any antiplatelet therapy + uncontrolled hypertension — treat hypertension first; compound risk is substantially elevated |
| Relative | Any antiplatelet therapy + diabetes + elevated BMI — triple additive risk; reduced shock wave parameters mandatory; vigilant post-procedure surveillance |
| Not a contraindication (with caution) | Low-dose aspirin monotherapy (75–150 mg/day) in Tier 1 patient — Regensburg evidence supports ESWL as an option with protocol modifications |
| Not a contraindication (with caution) | DAPT > 12 months from DES in Tier 2 patient — proceed with P2Y12 held per guideline timeline, aspirin continued, cardiology documented |
