So moving to our last speaker, it's a great privilege to introduce Dr. Nathaniel Smilowicz. He's an assistant professor in the Department of Medicine at the NYU Grossman School of Medicine, an interventional cardiologist at NYU, and he also serves as the principal investigator for an NIH, NHLBI study on coronary microvascular disease, and he's going to be speaking on M.I. in pregnancy. So Dr. Smilowicz, thank you so much. So today we're going to talk about myocardial infarction in pregnancy. These are my disclosures. None of them are directly relevant to the talk. So as we've already discussed, M.I. in pregnancy is a rare but potentially devastating complication of pregnancy, and in pregnancy-related M.I. diagnoses have been increasing over time. So this is a population-based study of 55 million pregnancy-related hospitalizations from 2002 to 2013, and you can see here that the rate of M.I. increased over time from 7 to about 9.5 per 100,000 hospitalizations. So it's rare, but it's potentially increasing in incidence. And M.I. is most common in the postpartum period. So in this cohort, we actually divided it into antepartum, labor and delivery, and postpartum hospitalizations, and you can see that 53% of the pregnancy-associated myocardial infarctions actually happen after the baby is born in the early postpartum period. Now, the M.I. incidence is highest in women who are older. So you can see here that the rate of M.I. in pregnancy is quite high in those who are age 40 and up, but even the cohort who's younger still has some incidence of myocardial infarction in pregnancy. And you can see here that actually 56% of myocardial infarctions occurred in pregnant women who are under the age of 35, so it didn't even meet the advanced maternal age threshold where we consider that the risks do go up during pregnancy. Now, we know that M.I. is associated with cardiovascular risk factors, and as you might expect, patients with tobacco use, hypertension, hypopedemia, diabetes, or renal disease have a substantially higher risk of M.I. during a pregnancy-associated hospitalization than those who do not. But 61% of pregnancy-associated M.I.s did occur in women without established CID risk factors, raising the importance of recognizing any risk factors prior to pregnancy and delivery and managing those risk factors, as we've already discussed. Now, a high proportion of M.I. in pregnancy are actually STEMI. Unlike non-pregnant women, where STEMI represents about 27% of myocardial infarctions, here you can see that STEMI represents 42% of M.I. in women, so there's a much higher risk of a total thrombosis versus the non-STEMI cohort. Now, pregnancy-associated mortality with M.I. is high, so in 4,471 pregnancy-associated myocardial infarctions, you can see that there was a 4.5% in-hospital mortality compared to a 0.01% in-hospital mortality in pregnancy hospitalizations without myocardial infarction. In this study, there was no significant difference between STEMI and non-STEMI mortality in these cohorts. But still, 5% mortality in a relatively healthy, young population is a devastating mortality rate. So now we've gone through the background of M.I. in pregnancy. How do you manage M.I. in pregnancy? This is obviously a challenging topic, and I won't belabor this point too much because this has been addressed by our prior speakers, but it's essential to highlight the importance of a team-based approach to the management of M.I. in pregnancy. Interdisciplinary care with obstetrics, MFM, interventional cardiology, but also critical care services, cardiac and labor and delivery nursing, cardiac and OB anesthesia, and potentially cardiothoracic surgery is important. The considerations for management of M.I. in pregnancy are complex. It involves making the right diagnosis, appropriate timing, medical management, invasive management, leading risks and radiation, and we'll touch on some of these topics. So with regard to diagnosis, what looks like an M.I. may not actually be a myocardial infarction. We have to keep in mind that pregnant women are at risk for pulmonary embolism, aortic dissection, Takotsubo syndrome, peripartum cardiomyopathy and acute decompensated heart failure, myocarditis, and preeclampsia and hypertensive urgency, which may all masquerade with the same signs and symptoms as myocardial infarction. Even among patients who do have M.I., there's a host of pathophysiologies that may be at play, including plaque rupture or erosion, spontaneous coronary artery dissection, which represents about 40% of M.I.s in pregnancy, in situ thrombosis or embolus given the hypercoagulable state of pregnancy, as well as coronary artery spasm. So all considerations that need to be taken into account. The timing of the M.I. clearly matters. So end-to-partum M.I., you need to consider fetal risks. During labor and delivery hospitalization, you need to consider both fetal and bleeding risks because the bleeding is a substantial concern in that time period. Whereas postpartum women, really they can be treated much more like a non-pregnant woman with an M.I. with the only caveat that the mechanism of M.I. may be substantially different with SCAD being much more common in the postpartum period. The medical management we touched on briefly, and I'll just review very quickly here, that antiplatelets and anticoagulation in pregnancy, aspirin is safe. There's limited data on P2Y12 safety, but there is quite an experience with copedigrel, and that is the preferred agent if a P2Y12 inhibitor needs to be administered. We do tend to shy away from pramsugol and ticagrelor, considering the bleeding risks and the absence of data with those meds. Heparin is safe and is the preferred anticoagulant if an invasive strategy is planned. Bromeliasis should be avoided. I think that goes without saying. It does not cause the placenta, but can cause subplacental bleeding complications and can be devastated. Other key therapies for M.I. are also likely safe. You can give beta-blockers, metoprolol and carbetolol, diuretics such as furosemide, nitrates, nitroglycerin, as well as morphine and opiates and benzodiazepines as needed for sedation during the procedure. Some therapies are contraindicated in pregnancy, and I think this needs to be reiterated, that statins, ACE inhibitors, ARBs, aldosterone antagonists, and SGLT2 inhibitors should not be used in pregnant patients. This is a consideration in those who've had a recent M.I. when you're considering discharge medications. The question of invasive management is a challenging one, and I think that we've addressed this to some degree. Who do you refer for invasive management? Well, clearly all STEMIs should go straight for invasive management. Regardless of fetal concerns, you have to take care of the mother. NSTEMIs, you really can't think of as high risk or low risk. Patients who have refractory symptoms, heart failure, ischemic mitral regurgitation, hemodynamic instability, ventricular arrhythmias, or markedly elevated biomarkers should probably have an invasive strategy. In select, low-risk, stable patients with non-ST elevation acute myocardial infarction who have no ECG changes, resolved symptoms, very minimal cardiac biomarkers, and after shared decision-making, an ischemia-guided management strategy may be reasonable, watching those patients very closely to see if they have any recurrent symptoms. But I think that the overwhelming takeaway is that most of these patients should probably go for an invasive strategy to define their coronary anatomy. Concerns about the effects of ionizing radiation, as we've already reiterated, should not prevent or delay invasive management of M.I. once they begin. We've talked about abdominal shielding, short fluoro times, minimizing synangiography, low frame rates, collimation, and avoiding high magnification as strategies to reduce radiation to the fetus. And I'll skip this slide. Now, how often is invasive management performed? Well, in this large study of 4,400 pregnancy-associated M.I.s, only 53% of patients underwent an invasive strategy. And you can see that the frequency of an invasive strategy varied substantially depending on the time period in which the M.I. occurred. So, antepartum hospitalizations for myocardial infarction, about 43%, underwent invasive management. Those who were hospitalized for labor and delivery, only 24% who had a concomitant M.I. were managed invasively, whereas postpartum M.I.s, the majority of patients undergo an invasive strategy, although that 70% figure is still concerningly low, considering that 30% were treated conservatively. Among those invasively managed, 47% underwent coronary vascularization in this large cohort. And here you can see that 80% underwent PCI and 20% underwent CABG. And invasive management was associated with lower mortality, although these are heavily confounded observational data, so you have to take that with a big grain of salt. Now, what are the considerations during angiography for M.I.? Well, you should avoid deep catheter engagement during coronary cannulation, given the consideration and the risks for SCAD. Caution of Jackie and Tiger catheters, and maybe you guys can dive deep into the coronaries. Limit high-pressure contrast injections. And as we've already mentioned, if there's a viable gestational age, consider administration of antenatal corticosteroids. Fetal heart rate monitoring can be considered, and a standby obstetric team with a C-section kit and a warmer are prudent in case of the necessity for emergent cesarean delivery and maternal decompensation. Now, PCI and non-SCAD M.I. in pregnancy can generally be done, much as we do for non-pregnant women. Depth of the aspirin plavix, drug-eluting stents are preferred due to the durable patency, and in the setting of an embolic M.I., you can consider aspiration thrombectomy without a stent placement. If PCI is performed antepartum, the DAPT strategy needs to be considered carefully. So clopidogrel should be discontinued five to seven days prior to planned delivery because of the concerns of bleeding with narraxial anesthesia. You should continue low-dose aspirin in the peripartum period and consider bridging with IV heparin. There's limited data on the safety of Glycoprotein 2b3a or IV canker lower to bridge, but you can consider that in select cases, all acknowledging that there are risks of uncertainty in this area. How about for SCAD? SCAD is a different entity entirely. SCAD occurs anywhere from 15 to 40% of pregnancy-associated myocardial infarctions. It's attributed to hormonally-mediated vascular vulnerability and hemodynamic stressors, and it frequently occurs immediately following delivery, and most frequently in the first week after delivery of the baby. Factors associated with pregnancy-associated SCAD include advanced maternal age, black race, hypertension, dyslipidemia, anxiety, fibromuscular dysplasia, preeclampsia, migraines, fertility treatments, and multi-parity. These are all risk factors, although it's really, it is still hard to predict who's going to have SCAD. In a cohort of 120 patients with pregnancy-associated SCAD from case series published in the literature, 75% presented with STEMI. The LAD was involved in the majority, the left main in more than a third. Multi-vessel SCAD was present in 40%, and the ejection fraction was reduced in 44% of patients. PCI was done in this 120 patient registry or case series with only complete success of about 50%, with typical wiring and propagation of the dissection in quite a few of them. And outcomes of pregnancy-associated SCAD were poor, with shock in nearly a quarter, mechanical circulatory support required in about a quarter, and maternal mortality in 4%. So pregnancy-associated SCAD is not something to be trifled with. Conservative management is definitely the best approach, if it's feasible. SCAD often heals spontaneously with conservative management over the course of a few weeks. You should initiate beta blockers, monitor for quite a while as an inpatient after angiography to ensure no further propagation, and you can follow up after delivery with the coronary CTA to avoid recapping these patients. But if you have to intervene, you have to intervene. Unfortunately, PCI is associated with reduced likelihood of technical success with increased risks. And the considerations at the time of PCI should include careful wiring of atraumatic coronary guide wires, inter-coronary imaging to make sure you're in the true lumen, vessel fenestration can be considered with a low-pressure cutting balloon angioplasty, I should consider sending segments proximal to distal to limit the SCAD inflow and long stents to avoid SCAD propagation, and integrated dissection and re-entry techniques may be necessary if you're unable to access the true lumen. And of course, you want to make sure that you're in the true lumen, because if you stent into the false lumen, that's a devastating complication. Emergent CABG should be considered in select cases of multi-vessel SCAD involving the left main, LAD, and circumflex. Shock is common in these patients. They may require hemodynamic support, either ECMO or impella prior to the OR. And the surgical team should be aware that FMD can affect the lima and the rima if they're considering harvesting an arterial conduit, although this is obviously rare. It needs to be considered. Post-MI management, the optimal timing of delivery after MI is uncertain, and you need to individualize care. It probably should be postponed for two weeks after MI if that's feasible, though that's based on expert opinion. Vaginal delivery is generally preferable post-MI with lower bleeding complications and less hemodynamic shifts. And breastfeeding is not recommended in mothers who are taking anticoagulants other than low-dose aspirin. So to summarize, the management of MI in pregnancy is challenging. An invasive strategy should be performed in STEMI and all high-risk STEMIs. A conservative approach to management may be reasonable in some MI patients. Certainly once you make a diagnosis of SCAD, if there's non-active ischemia and the patient's hemodynamically stable, a conservative approach is preferred. And it's essential to coordinate care between obstetric and cardiovascular teams, that team-based care will improve outcomes. And that is what I have on this very interesting and challenging topic. Thanks for the opportunity to present today. Thank you so much, Dr. Smolets. That was really fantastic. And I know that I've talked with many of my interventional colleagues, and I think that one of the reasons we wanted to have this webinar was to address a variety of topics that are often every interventional's worst nightmare in terms of being called to assess a pregnant patient. So thank you so much for addressing many of those topics.

myocardial infarction

pregnancy

M.I.

postpartum period

cardiovascular risk factors