Chest Pain in the Patient with a Left Ventricular Assist Device

 

Chest Pain in the Patient with a Left Ventricular Assist Device: A Paradigm Shift in Cardiovascular Assessment

Dr Neeraj Manikath , claude.ai

Abstract

Left ventricular assist devices (LVADs) represent a life-saving therapy for advanced heart failure, yet they fundamentally alter cardiovascular physiology in ways that challenge conventional medical assessment. The continuous-flow LVAD creates a pulseless circulation with unique hemodynamic parameters that render traditional approaches to chest pain evaluation obsolete. This review provides internists and emergency physicians with a framework for understanding LVAD physiology, recognizing true emergencies, and managing acute presentations in this growing patient population. We emphasize that chest pain in LVAD patients rarely represents myocardial ischemia in the conventional sense, but may herald life-threatening complications requiring immediate recognition.

Introduction

The landscape of advanced heart failure management has been transformed by mechanical circulatory support. Over 30,000 patients worldwide currently live with LVADs, and every internist will encounter these patients in emergency departments, hospital wards, and outpatient settings.1,2 Yet medical education has not kept pace with this reality. Most physicians remain unfamiliar with the altered physiology of continuous-flow devices and the completely different approach required when these patients present with chest discomfort.

The third-generation continuous-flow LVADs (HeartMate 3, HeartWare HVAD) operate at 2,000-10,000 rpm, creating non-pulsatile flow that fundamentally changes every aspect of cardiovascular assessment we learned in medical school.3 These patients have no palpable pulse, blood pressure must be measured with Doppler ultrasound, and the physical examination bears little resemblance to traditional cardiology teaching. Most importantly, "chest pain" in LVAD patients represents an entirely different differential diagnosis than in the general population.

Pearl #1: The LVAD patient is a hemodynamic paradox—they may have severe coronary disease yet present without classic angina because their native left ventricle is mechanically unloaded and oxygen demand is minimal.

Understanding LVAD Physiology: Why Everything Changes

The Mechanics of Continuous Flow

Modern LVADs are implanted in the left ventricular apex and pump blood continuously into the ascending aorta at flows of 4-6 L/min.4 This creates several profound physiological alterations:

  1. Ventricular Unloading: The native left ventricle is decompressed, with minimal wall stress and dramatically reduced myocardial oxygen consumption. The ventricle often becomes atrophied and contributes little to cardiac output.5

  2. Absent Pulsatility: Continuous flow means no arterial pulse wave. The aortic valve rarely opens. Mean arterial pressure (MAP) typically ranges from 70-90 mmHg, but there is minimal pulse pressure.6

  3. Altered Coronary Perfusion: Coronary blood flow, normally dependent on diastolic pressure gradients, becomes continuous rather than phasic. This changes ischemia dynamics fundamentally.7

Pearl #2: In a well-functioning LVAD, the native heart contributes only 10-20% of total cardiac output. The device is doing the work, not the myocardium.

Can LVAD Patients Have a STEMI?

The short answer: not in the conventional sense.

While coronary occlusion can certainly occur, the clinical presentation and consequences differ dramatically from typical acute coronary syndrome.8 Here's why:

  • The unloaded, atrophied left ventricle has minimal oxygen demand
  • Transmural infarction may occur without hemodynamic collapse
  • ECG changes are often absent or uninterpretable due to prior cardiomyopathy
  • Classic crushing substernal chest pain is rare because wall stress is minimal

Instead, acute myocardial ischemia in LVAD patients manifests as:

  • Ventricular arrhythmias (VT/VF) from scar or acute injury
  • Device flow alarms from reduced ventricular filling
  • Right ventricular failure (the RV is not supported by the device)
  • Subtle hemodynamic deterioration rather than dramatic chest pain9

Oyster #3: If an LVAD patient develops chest pain, think device complications FIRST, cardiac ischemia second. The reverse priority from your usual approach.

The LVAD Physical Examination: Relearning the Basics

What You Won't Find

  • No radial or carotid pulse (though 10-20% may have a weak, thready pulse if native ventricle contributes)
  • No standard blood pressure by automatic cuff (reads "error")
  • Heart sounds? A continuous mechanical hum at 2-10 kHz

What You Must Assess

1. The Device Controller This small external computer is the patient's lifeline. Key parameters:10

  • Speed (RPM): Typically 4,800-5,400 rpm for HeartMate 3
  • Flow: Target 4-6 L/min at rest
  • Power: Usually 4-8 watts
  • Pulsatility Index (PI): The holy grail—reflects native ventricular contribution
    • Normal PI: 4-7
    • Low PI (<3): Suggests hypovolemia, tamponade, or RV failure
    • High PI (>10): Possible suction event or outflow obstruction11

Pearl #4: The pulsatility index is your CVP, wedge pressure, and cardiac output rolled into one. A dropping PI with rising power consumption screams pump thrombosis.

2. Mean Arterial Pressure Requires Doppler ultrasound or manual palpation method:12

  • Place Doppler probe over brachial artery
  • Inflate cuff until humming sound disappears
  • Slowly deflate—the pressure when sound returns is the MAP
  • Target MAP: 70-90 mmHg

3. Right Heart Assessment The Achilles heel of LVAD patients. The device supports only the left ventricle; RV failure is catastrophic.13

Signs of RV dysfunction:

  • Elevated jugular venous pressure (>12 cm H2O)
  • Hepatomegaly with positive hepatojugular reflux
  • Peripheral edema
  • Ascites
  • Declining LVAD flows despite adequate MAP

Hack #5: If JVP is elevated with low device flows, think RV failure, not volume overload. Diuresis may worsen hemodynamics by reducing preload.

The True LVAD Emergencies: A Different Differential

When an LVAD patient presents with chest discomfort or dyspnea, the differential diagnosis is radically different:14

1. Pump Thrombosis (Incidence: 8-15%)

The nightmare scenario. Blood clots form on the impeller, increasing friction and hemolysis.15

Clinical Presentation:

  • Subacute dyspnea, chest pressure (from pulmonary edema)
  • Dark "Coca-Cola" urine (hemoglobinuria)
  • Device controller shows: ↑ power, ↓ flow, ↓ PI
  • Labs: ↑↑ LDH (>1000 U/L), ↑ plasma-free hemoglobin, ↓ haptoglobin, ↑ total bilirubin

Pearl #6: LDH >1000 U/L in an LVAD patient is pump thrombosis until proven otherwise. This trumps every other diagnosis.

Emergency Management:

  • Contact LVAD center immediately
  • Check anticoagulation (INR target 2-3)
  • Obtain: CBC, complete metabolic panel, LDH, plasma-free Hb, haptoglobin
  • Do NOT adjust device settings without expert guidance
  • Urgent admission for possible thrombolysis or device exchange16

2. Driveline Infection (Incidence: 20-40%)

The percutaneous driveline is a direct conduit to the device and bloodstream.17

Clinical Signs:

  • Erythema, purulence, or tenderness at exit site
  • Fever with positive blood cultures (often Staph aureus)
  • Chest pain if infection tracks to pump pocket

Management:

  • Blood cultures, wound cultures
  • CT chest if pocket infection suspected
  • Prolonged IV antibiotics (6-8 weeks minimum)
  • Surgical debridement often required18

3. Gastrointestinal Bleeding (Incidence: 20-40%)

Loss of pulsatile flow causes acquired von Willebrand syndrome and intestinal arteriovenous malformations.19

Presentation:

  • Melena or hematochezia (rarely hematemesis)
  • Anemia often profound
  • May present as dyspnea from anemia, not obvious bleeding

Hack #7: GI bleeding in LVAD patients is notoriously difficult to localize. Anticipate multiple endoscopies and consider video capsule endoscopy early.

4. Right Ventricular Failure

The device unmasks or worsens RV dysfunction by increasing venous return to an already failing right heart.20

Triggers: Volume overload, pulmonary hypertension, RV infarction, arrhythmias

Signs: Elevated JVP, hepatomegaly, peripheral edema, LOW device flows

Management:

  • Diuretics (cautiously—may reduce LVAD preload)
  • Inotropes (milrinone, dobutamine)
  • Pulmonary vasodilators if pulmonary hypertension
  • Avoid excessive fluid resuscitation21

Special Scenarios: When LVADs Code

Cardiac Arrest in the LVAD Patient

Oyster #8: Yes, you START CPR. Immediately. The device can withstand compressions, but the brain cannot tolerate no flow.

The evidence is clear: delayed CPR in LVAD patients increases mortality.22 Guidelines from INTERMACS (Interagency Registry for Mechanically Assisted Circulatory Support):

**Immediate Actions:**23

  1. Start high-quality CPR (device will alarm—ignore it)
  2. Call the LVAD coordinator and VAD center emergently
  3. Check device controller: Is it displaying parameters?
    • If "RED HEART" symbol: Check driveline connection, change batteries
    • If functioning: Continue CPR, treat underlying rhythm
  4. Defibrillate if VT/VF (device is protected)
  5. Standard ACLS medications

Pearl #9: The device may be working perfectly, but VF means no coronary or cerebral perfusion. They need CPR just like anyone else.

Troubleshooting Device Alarms

Alarm Meaning Action
Low Flow Suction, hypovolemia, RV failure Give fluids, assess RV function
High Power Pump thrombosis, outflow obstruction Check LDH, call VAD team
Red Battery <15 minutes power Change batteries immediately
Disconnected Driveline Self-explanatory Reconnect, ensure seated properly

Diagnostic Approach: A Stepwise Framework

When faced with chest pain/dyspnea in an LVAD patient:24

Step 1: Assess Device Function

  • Controller parameters (speed, flow, power, PI)
  • Battery life adequate?
  • Any alarms?

Step 2: Hemodynamic Assessment

  • MAP by Doppler (target 70-90)
  • Estimate central venous pressure (JVP)
  • Signs of RV failure vs LV failure

Step 3: Directed Laboratory Testing

  • CBC, CMP, LDH, plasma-free Hb (if concern for thrombosis)
  • Troponin (often chronically elevated, trending more useful)
  • BNP (limited utility in chronic device patients)
  • Blood cultures if febrile

Step 4: Imaging

  • CXR: Device position, pulmonary edema, pneumonia
  • Echocardiography: RV function, aortic valve (should be closed), LV size
  • CT chest: If concern for driveline/pocket infection
  • Coronary angiography: Rarely indicated emergently unless device function ruled out

Hack #10: Don't reflexively order a troponin. It's chronically elevated from device-related hemolysis and myocardial stretch. Trends over days matter more than absolute values.

Special Considerations: Anticoagulation

All LVAD patients require lifelong anticoagulation to prevent pump thrombosis, typically:25

  • Warfarin (target INR 2-3 for HeartMate 3)
  • Aspirin 81-325 mg daily

Bleeding complications are common (GI bleeding, stroke, epistaxis), creating a narrow therapeutic window.

For invasive procedures:

  • Target INR 1.5-2.0 for most procedures
  • Never completely discontinue anticoagulation
  • Bridge with heparin for high-risk procedures26

Long-Term Management Pearls

Beyond acute presentations, LVAD patients require meticulous outpatient management:27

  1. Infection Prevention: Driveline site care daily, avoid swimming
  2. Medication Adherence: Especially anticoagulation—pump thrombosis is often fatal
  3. Device Alarms: Patients must respond immediately, never ignore
  4. Avoid Magnetic Fields: MRI generally contraindicated, airport security requires special card
  5. Psychological Support: Depression and anxiety are prevalent

Pearl #11: LVAD patients should carry their controller manual, emergency card with VAD center contact, and spare batteries at all times. Make this a discharge checklist item.

Conclusion: A New Paradigm

Chest pain in the LVAD patient demands a cognitive shift from traditional cardiology thinking. These patients inhabit a unique physiological state where:

  • Ischemia rarely presents as angina
  • Device complications masquerade as cardiac symptoms
  • Physical examination requires relearning fundamental skills
  • Emergencies require immediate contact with specialized teams

The internist's role is not to manage the LVAD (that requires specialized training), but to recognize when device complications are causing symptoms and activate the appropriate resources urgently. In the era of mechanical circulatory support, understanding LVAD physiology is no longer optional—it's essential medicine.

Final Oyster: When in doubt, call the VAD center. They are available 24/7 and would rather receive ten unnecessary calls than miss one pump thrombosis.

References

  1. Kirklin JK, Pagani FD, Kormos RL, et al. Eighth annual INTERMACS report. J Heart Lung Transplant. 2017;36(10):1080-1086.

  2. Mehra MR, Naka Y, Uriel N, et al. A fully magnetically levitated circulatory pump for advanced heart failure. N Engl J Med. 2017;376(5):440-450.

  3. Slaughter MS, Rogers JG, Milano CA, et al. Advanced heart failure treated with continuous-flow left ventricular assist device. N Engl J Med. 2009;361(23):2241-2251.

  4. Feldman D, Pamboukian SV, Teuteberg JJ, et al. The 2013 International Society for Heart and Lung Transplantation Guidelines for mechanical circulatory support. J Heart Lung Transplant. 2013;32(2):157-187.

  5. Drakos SG, Janicki L, Horne BD, et al. Risk factors for right ventricular failure after left ventricular assist device implantation. Am J Cardiol. 2010;105(7):1030-1035.

  6. Uriel N, Sayer G, Addetia K, et al. Hemodynamic ramp tests in patients with left ventricular assist devices. JACC Heart Fail. 2016;4(3):208-217.

  7. Cornwell WK, Tarumi T, Stickford A, et al. Effect of pulsatile and nonpulsatile flow on cerebral perfusion in patients with left ventricular assist devices. J Heart Lung Transplant. 2014;33(12):1295-1303.

  8. Cowger J, Pagani FD, Haft JW, et al. The development of aortic insufficiency in left ventricular assist device-supported patients. Circ Heart Fail. 2010;3(6):668-674.

  9. Topkara VK, Kondareddy S, Malik F, et al. Infectious complications in patients with left ventricular assist device: etiology and outcomes in the continuous-flow era. Ann Thorac Surg. 2010;90(4):1270-1277.

  10. Estep JD, Starling RC, Horstmanshof DA, et al. Risk assessment and comparative effectiveness of left ventricular assist device and medical management. J Am Coll Cardiol. 2015;66(16):1747-1761.

  11. Uriel N, Morrison KA, Garan AR, et al. Development of a novel echocardiography ramp test for speed optimization and diagnosis of device thrombosis in continuous-flow left ventricular assist devices. J Am Coll Cardiol. 2012;60(18):1764-1775.

  12. Bennett MK, Adatya S. Blood pressure management in mechanical circulatory support. J Thorac Dis. 2015;7(12):2125-2128.

  13. Lampert BC, Teuteberg JJ. Right ventricular failure after left ventricular assist devices. J Heart Lung Transplant. 2015;34(9):1123-1130.

  14. Stulak JM, Maltais S, Cowger J, et al. Prevention of percutaneous driveline infection after left ventricular assist device implantation. Ann Cardiothorac Surg. 2014;3(6):627-630.

  15. Starling RC, Moazami N, Silvestry SC, et al. Unexpected abrupt increase in left ventricular assist device thrombosis. N Engl J Med. 2014;370(1):33-40.

  16. Goldstein DJ, John R, Salerno C, et al. Algorithm for the diagnosis and management of suspected pump thrombus. J Heart Lung Transplant. 2013;32(7):667-670.

  17. Hannan MM, Husain S, Mattner F, et al. Working formulation for the standardization of definitions of infections in patients using ventricular assist devices. J Heart Lung Transplant. 2011;30(4):375-384.

  18. Nienaber JJ, Kusne S, Riaz T, et al. Clinical manifestations and management of left ventricular assist device-associated infections. Clin Infect Dis. 2013;57(10):1438-1448.

  19. Crow S, Chen D, Milano C, et al. Acquired von Willebrand syndrome in continuous-flow ventricular assist device recipients. Ann Thorac Surg. 2010;90(4):1263-1269.

  20. Kormos RL, Teuteberg JJ, Pagani FD, et al. Right ventricular failure in patients with the HeartMate II continuous-flow left ventricular assist device. J Thorac Cardiovasc Surg. 2010;139(5):1316-1324.

  21. Grant AD, Smedira NG, Starling RC, Marwick TH. Independent and incremental role of quantitative right ventricular evaluation for the prediction of right ventricular failure after left ventricular assist device implantation. J Am Coll Cardiol. 2012;60(6):521-528.

  22. Haglund NA, Davis ME, Tricarico NM, Keebler ME. Cardiovascular resuscitation in patients with a left ventricular assist device. Curr Cardiol Rev. 2014;10(2):166-171.

  23. Peberdy MA, Gluck JA, Ornato JP, et al. Cardiopulmonary resuscitation in adults and children with mechanical circulatory support. Circulation. 2007;116(24):2664-2676.

  24. Cheng A, Williamitis CA, Slaughter MS. Comparison of continuous-flow and pulsatile-flow left ventricular assist devices. J Thorac Cardiovasc Surg. 2014;148(2):573-577.

  25. Netuka I, Ivák P, Tuček L, Gregor S. Evaluation of von Willebrand factor with a fully magnetically levitated centrifugal continuous-flow left ventricular assist device in advanced heart failure. J Heart Lung Transplant. 2016;35(7):860-867.

  26. Aggarwal A, Pant R, Kumar S, et al. Incidence and management of gastrointestinal bleeding with continuous flow assist devices. Ann Thorac Surg. 2012;93(5):1534-1540.

  27. Pagani FD, Miller LW, Russell SD, et al. Extended mechanical circulatory support with a continuous-flow rotary left ventricular assist device. J Am Coll Cardiol. 2009;54(4):312-321.

Author Note: This review is intended for educational purposes to prepare internists for the growing population of LVAD patients. All clinical decisions should be made in consultation with the patient's VAD center and multidisciplinary team.

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