MTC 9/13: Slip into something comfortable and come learn about hyperlipidemia!

During our primary care conference this morning, we tackled the subject of hyperlipidemia in young adults. Our wonderful R2 Dr. Preethi Venkat presented the case of a healthy woman in her 20s with no family history of premature atherosclerotic cardiovascular disease (ASCVD) who was found to have fasting LDL levels of greater than 190 mg/dL.

While the US Preventive Services Task Force (USPSTF) concludes that there is insufficient evidence to recommend lipid screening in individuals under the age of 40, the American Heart Association and American College of Cardiology state that it is reasonable to screen individuals ages 20-39 every 4-6 years, depending on their risk factors. Armed with this information and with help from our primary care expert Dr. Jeffrey Jenks, we developed an algorithm for determining which patients should be started on statin therapy for primary prevention of ASCVD events.

  • LDL ≥ 190: Patients with LDL ≥ 190 mg/dL should receive high-intensity statin therapy regardless of their age.
  • All patients ages 40-75 with diabetes mellitus: These patients should receive moderate- or high-intensity statin therapy depending on their ASCVD risk, including whether “risk enhancers” are present (see below).
  • High-risk patients ages 20-39 with diabetes mellitus: Moderate-intensity statin therapy can be considered in these patients if “risk enhancers” are present: long duration (type 2 for 10 years or type 1 for 20 years), microvascular disease (nephropathy, retinopathy, or neuropathy), or ankle-brachial index (ABI) < 0.9.
  • Patients ages 40-75 with an elevated 10-year ASCVD risk: A 10-year ASCVD risk should be estimated using validated calculators, and the results should be used to guide therapy (high-intensity statin if risk ≥ 20%, moderate- or high-intensity statin if risk is 7.5-20%, and consider moderate-intensity statin if risk is 5-7.4%).
  • Patients ages 20-39 with LDL ≥ 160 and family history of premature ASCVD or genetic dyslipidemia: It may be reasonable to initiate moderate-intensity statin in these patients after weighing of risks and benefits.

Remember that lifestyle counseling is indicated in every patient with increased ASCVD risk. Younger patients are often reluctant to start pharmacotherapy. As the benefits of primary prevention of ASCVD are long-term (10-year NNT 30 for moderate-intensity statin therapy and 20 for high-intensity statin therapy), it may be reasonable to repeat a fasting lipid profile in 3-6 months before initiating therapy. Lastly, for patients with borderline to intermediate 10-year ASCVD risk (5-19.9%), coronary artery CT angiogram may be used to guide the decision to initiate statin therapy.

Thank you so much to Dr. Jenks and Dr. Venkat for another successful primary care morning report!

Medical Spanish Word of the Day: el colesterol = cholesterol

MTC 8/2: A Generous Heart – Acute Pericarditis with Effusion

During our morning report at Hillcrest today, we discussed the case of an otherwise healthy young man who presented to the ED with positional chest pain, dyspnea, and diffuse ST elevations and PR depressions on EKG. He was diagnosed with acute pericarditis and discharged home with ibuprofen and colchicine. However, two weeks later, he returned to the hospital with worsening symptoms and was found to have a large pericardial effusion and signs of early cardiac tamponade. He required pericardial drain placement and was admitted for observation. He was ultimately treated with prednisone and celecoxib and was also started on rilonacept (an IL-1 decoy receptor newly approved by the FDA to treat recurrent pericarditis) to reduce his risk of recurrence.

Dr. Al Khiami, one of our interventional cardiologists, helped us review the diagnostic criteria and management of acute pericarditis. We talked about several exam findings that can be seen in pericarditis and tamponade: pericardial rub, pulsus paradoxus (systolic BP drop of >10 mmHg with inspiration), and Beck’s triad (hypotension, JVD, muffled heart sounds). We also discussed the classic EKG changes associated with pericarditis (diffuse ST elevation and PR depression) and tamponade (electrical alternans). Findings on echocardiogram suggestive of tamponade include: diastolic RV collapse (specific), systolic RA collapse (earliest sign), plethoric IVC with minimal respiratory variation (sensitive), and exaggerated respiratory cycle changes in mitral/tricuspid valve in-flow velocities (echocardiographic equivalent of pulsus paradoxus).

We would like to thank Dr. Al Khiami for taking time out of his busy schedule to join us today!

Medical Spanish Word of the Day: la pericarditis con efusión = pericarditis with effusion

Clinical Reasoning Conference – July 2021

For our first Clinical Reasoning Conference of the academic year, our expert diagnostician was the incomparable Dr. Lori Daniels, cardiologist extraordinaire and a former chief resident of our program. Dr. Daniels walked us through the mystery case of a relatively healthy young woman who presented with acute-onset, sharp midsternal chest pain and was found to have dynamic EKG changes, elevated cardiac biomarkers, and apical hypokinesis on echocardiogram. A computed tomography of the coronary arteries showed abrupt tapering of the mid- to distal left anterior descending artery, which was consistent with spontaneous coronary artery dissection (SCAD). With treatment and cardiac rehabilitation, the patient had a good cardiac recovery. She was ultimately diagnosed with an arteriopathy.

We took this opportunity to discuss the uncommon but important diagnosis of SCAD, caused by hematoma formation within the tunica media, which then leads to intimal separation from the underlying vessel. Triggers include stress, Valsalva, intense exercise, hormonal changes, and medications. Most cases occur in young women with few traditional cardiac risk factors. SCAD can be associated with pregnancy and can occur in the postpartum setting. SCAD can present similarly to other causes of acute coronary syndrome (ACS), with typical chest pain, elevated cardiac biomarkers, EKG changes (including ST segment elevations), and wall motion abnormalities. Most cases are diagnosed through cardiac catheterization. Thrombolytics are generally avoided as they may cause extension of the dissection or hematoma. The role of antiplatelet agents and anticoagulants in SCAD is unclear, but these agents are often given. Neurohormonal block with β-blockers and ACE inhibitors (or ARBs) is also typically initiated. Percutaneous coronary intervention and coronary artery bypass graft surgery may be appropriate in select patients.

We were fortunate to have been joined by the patient, who shared her unique perspective on the experience. The classic teaching that women with ACS tend to present atypically is flawed. Studies suggest that women who have ACS report typical chest pain at similar rates as men who have ACS. Although women have higher rates of insurance and primary care than men, women who develop ACS report more difficulty receiving care than their male counterparts. In addition, despite having a higher cardiac risk burden and risk of severe myocardial infarction, women who have ACS are less likely to be appropriately diagnosed on presentation and less likely to be reperfused in a timely manner. Indeed, health inequities related to sex and other social determinants of health remain pervasive today.

Key Learning Points:

  1. SCAD is an important cause of acute coronary syndrome, particularly in young women who have few traditional cardiovascular risk factors.
  2. Not all chest pain is from atherosclerotic plaque rupture. Consider other diagnoses such as aortic dissection, pulmonary embolism, pneumothorax, and SCAD.
  3. In SCAD, most medications used to treat other causes of acute coronary syndrome can be delayed and administered after an angiogram without significant issues.
  4. Discrepancies related to sex and other social determinants of health in the management of individuals who present with chest pain remain commonplace.

Thank you to Dr. Daniels and our other expert discussants for participating in our conference today!

MI or Pericarditis? I dunno…

We’re continuing to practice our clinical skills with a daily ECG! Today’s diagnosis: acute pericarditis. Two aspects of the ECG point to this diagnosis: 

  1. Diffuse ST elevations (leads I, II, III, aVF, V3-V6) indicated by arrows. In myocardial infarction the ST elevations tend to be localized (inferior, anterior, posterior, lateral), often with reciprocal ST depressions. 
  2. PR segment displacement indicated by asterisks. PR elevation can be seen in aVR and PR depression are seen in leads II, aVF, V4-V6.

Morning Report – Tuesday 12/29 at the VA!

Tuesday morning report at the VA was all about diuretics. We presented a case of a 73-year-old man with history of CHF, CKD and T2DM who presented with progressive dyspnea, bilateral lower extremity swelling, orthopnea, and abdominal distension. Physical exam showed evidence of volume overload with 3+ pitting edema, elevated JVD, and bibasilar pulmonary crackles. We considered various common triggers of heart failure exacerbation before diving into a discussion of diuretics. 

Key points that we highlighted:

  • Decongestion with resolution of symptoms and edema is achieved through “diuresis” = loss of sodium (natriuresis) + loss of water (diuresis). That is why sodium-limited diet is crucial in treatment of fluid overload. 
  • Loop diuretics function as “threshold” drugs that need to achieve a sufficient concentration in order to work. The natriuretic threshold is higher in patients with acute CHF than in healthy persons. That is why hospitalized patients require loop diuretic doses that are higher than stable outpatient doses.
  • Loop diuretics exhibit a “ceiling” effect and doses above the ceiling will not increase the amount of natriuresis. Acute CHF shifts the relation between plasma diuretic concentration and sodium excretion to the right and reduces the “ceiling.” 
  • Patients with chronic diuretic use develop post-diuretic sodium retention and decreased efficacy with each subsequent loop diuretic dose. That is why loop diuretics are dosed multiple times daily and why patients need a net negative sodium balance each day. 
  • Chronic loop diuretic use leads to distal tubular hypertrophy and once maximum loop diuretic effect is reached, auxiliary diuretics are sometimes used (thiazide, aldosterone antagonists, carbonic anhydrase inhibitors). We discussed specific situations you may consider using these agents. 
  • Ethacrynic acid is the loop diuretic of choice in patients with sulfa allergy. 

For further reading, check out this review from the NEJM: 

Ellison DH, Felker GM. Diuretic Treatment in Heart Failure. N Engl J Med. 2017 Nov 16;377(20):1964-1975.

MTC – Cardiotoxicity of Cancer Therapeutics

This morning, second year Med-Peds resident Nicky Herrick presented a great case female who presented with progressive sub acute shortness of breath. The patient’s past medical history notably included breast cancer they had been treated seven years prior with a chemotherapeutic regimen containing doxorubicin and trastuzumab. The patient was admitted to the hospital and initial work up revealed a new onset ectopic rhythm, volume overload, and pulmonary edema. Patient underwent a transthoracic echocardiogram (TTE), which demonstrated a severely depressed left ventricular ejection fraction, but no significant focal wall motion abnormalities. A CT chest with contrast was negative for pulmonary embolism. A coronary angiogram was completed showing no obstructive coronary disease. The ideology of the patient’s heart failure presentation was felt to be due to a combination of anthracycline and TKI induced cardiomyopathy.

We reviewed the broad classes of cancer therapeutics and their potential for cardiotoxicity: Screen Shot 2020-04-07 at 10.46.56 AM.png

While focusing on anthracycline toxicity, which is thought to be due to a the formation multimeric complex of DNA, anthracycline, and Topoisomerase causing DNA instability and subsequent cardiac myocyte apoptosis, we discussed that one of the most important determinants of whether patients would be susceptible to the short and longer term risks of cardiomyopathy are the cumulative dose of the anthracycline. It is important to know that these cumulative doses are additive across different types of anthracyclines as well. ASCO has published guidelines to help identify those patients who are at increased risk:

Screen Shot 2020-04-07 at 10.53.22 AM.png

Finally, while anthracycline toxicity was traditionally thought to manifest in an early phase (causing dysrhythmias) and a chronic phase (causing CHF and cardiomyopathy), more recent literature suggests that LV dysfunction occurs early following exposure to such agents and adopts a indolent irreversible course. In a single prospective cohort study, ~30% of patients who received an anthracycline based chemotherapeutic regimen developed LV dysfunction as detected by surveillance TTEs done q3 months. 98% of those patients developed the dysfunction within the first year, bringing into question whether prior dogma of early and late phases of anthracycline mediated cardiomyopathy may have been a reflection of a lack of standardized monitoring, rather than a true bimodal distribution of disease.

Take Home Points: 

  1. A variety of chemotherapeutic drugs: anthracyclines, taxanes, tyrosine kinase inhibitors, checkpoint inhibitors, alkylating agents can all cause different forms of cardiotoxicity. As patients begin to live longer with more advanced chemotherapeutic options, clinicians will need to be aware of the downstream side effects that may limit patient’s survival long term.
  2. Combinations of anthracyclines with TKIs and/or radiation to the cardiac bed may potentiate the risks of cardiotoxicity in cancer patients.
  3. The traditional canon of different phases of anthracycline induced cardiomyopathy may occur early and more insidiously than previously thought due to closer monitoring of LV function.

Thank you Nicky for a great case, and thank you to Jason Duran for your expert input!

Morning Report 3/30: PRES

Today our amazing R3 Allen Jiang led us through a case of a elderly man with a history of HTN, HFpeEF, Afib and DM who came in with SOB and was found to have severe hypertension.

He had a headache and then developed respiratory failure and had a seizure and thus we were concerned for hypertensive emergency specifically for an intracranial process such as PRES.

We went over the classifications for severe hypertensive and also the mechanism of autoregulation for blood pressure for the brain to remind of how end-organ damage may manifest itself there.

Our expert discussant, Dr. Sean Evans reminded us that when BP is ultimately controlled, one might expect neurological recovery to occur within days to months, but rarely PRES is not actually reversible or there may be recurrent seizures.

Take Away Points:

  1. PRES stands for posterior reversible encephalopathy syndrome, and is commonly associated with hypertensive emergency as well as pre-eclampsia/eclampsia as well as cytotoxic or immunosuppresive agents.
  2. One might see white matter changes/ areas of edema on MRI specifically in the posterior or occipital regions of the brain but it is not present in all patients
  3. Use IV labetalol or nicardipine as first line agents when treating HTN in PRES to lower the blood pressure carefully. Aim for 25% reduction in first 4 hours, as the blood pressure set point for hypotensive injury is much higher in patients with chronic hypertension!

Thanks again, Dr. Evans for your clinical pearls and to Dr. Jiang for a great case!

HC MTC – Coronary Subclavian Steal Syndrome

This morning we discussed the case of an elderly female who had a history of CAD and received a coronary artery bypass graft surgery nearly a decade ago, who presented with atypical chest pain, left arm numbness and tingling. Her admission work up revealed dynamic ECG findings indicative of ongoing ischemia and a transthoratic echocardiogram revealed new left ventricular dysfunction with a reduced ejection fraction. The patient underwent a coronary angiogram, which revealed native three-vessel disease, but patent bypass grafts. However, a 90% subclavian stenosis was visualized, as well as retrograde flow was visualized in the LIMA to LAD graft, suggestive of coronary subclavian steal syndrome. lily_ch32_f006.png

We discussed the pathophysiology of this relatively rare complication, as well as the pertinent anatomy. Proximal left sided subclavian stenoses >75% are more likely to predispose patients to this phenomenon. However alongside left upper extremity symptoms such as claudication, paresthesias, numbness, weakness, and/or skin/temperature changes, there is an additional risk of vertebrobasilar ischemia given the location of the left vertebral artery that also sits distal to the region of stenoses. Symptoms that would be indicative of vertebrobasilar ischemia may include lightheadedness, presyncope, vertigo, ataxia, visual deficits, among other neurologic signs.

The patient underwent subclavian artery stenting, which ultimately relieved her extremity symptoms as well as her angina. Please see below.

 

Take Home Points:

  • Keep high index of suspicion for ischemia, particularly as females are more likely to present with atypical symptoms
  • Be aware of extra-coronary lesions that may result in hemodynamic changes to the coronary circulation. Coronary subclavian steal syndrome is a rare, but intervenable complication following CABG in patients with high grade subclavian stenoses

HC MTC 2/27: Chagas cardiomyopathy

Today in Hillcrest, we discussed a patient with end-stage heart failure who was found to have RBBB+LAFB and an EF of 13%. We took this opportunity to review the conduction system, and EKG findings for bundle branch pathologies. After ruling out ischemic disease, we also explored possible etiologies for his non-ischemic cardiomyopathy with the acronym HIVEMIND (coined by CMR Gary Ma). A thorough history was key in eliminating many of the possible etiologies, and the key was his immigration from El Salvador which prompted testing for Chagas! He was ultimately diagnosed with Chagas cardiomyopathy and underwent cardiac transplantation. However, his story did not end there. After reviewing the illness script for cardiac manifestations of Chagas, which include arrhythmias, cardiomyopathy, and aneurysms, we learned that post-transplant patients still need to be regularly monitored the disease given the possibility of reactivation. This patient had not one, but two recurrences of his Chagas disease with significant conduction system disease (RBBB, 2:1 AV block) requiring multiple treatments with benznidazole and pacemaker placement!

Thank you to our discussant Dr. Anna McDivit for her insights on approaching bundle branch blocks, and for reminding us to have a lower threshold for ICD implantation in Chagas cardiomyopathy patients given their high risk for fatal arrhythmias! Thanks also to Dr. Gary Ma for his clever acronym for NICM.

Takeaway points:

  1. Prolonged QRS intervals should prompt consideration of a bundle branch block, while axis deviations should prompt consideration of fascicular blocks.
  2. The differential for non-ischemic cardiomyopathy is broad (think HIVEMIND!) – start with a comprehensive history to guide further testing.
  3. Chagas disease is the most common etiology of non-ischemic cardiomyopathy in Central America. Consider Chagas disease in any patient with cardiac symptoms or EKG abnormalities from a Chagas-endemic area (particularly immigrants from El Salvador or southern Mexico). RBBB+LAFB is the most common conduction abnormality, though any can occur.
  4. Chagas disease has an acute and chronic phase. First-line treatment for Chagas disease is benznidazole, although treatment is less effective for chronic infections.
  5. Cardiac transplant is indicated in patients with Chagas cardiomyopathy and end-stage heart failure. Post-transplant patients must be monitored for disease reactivation.