Gulati, Rajiv

Background Mental health after spontaneous coronary artery dissection ( SCAD ), a cause of myocardial infarction in young women, remains largely unexplored. We assessed the prevalence and severity of psychiatric symptoms after SCAD . Methods and Results Individuals with confirmed SCAD who consented to the Mayo Clinic “Virtual” Multicenter SCAD Registry were sent the Posttraumatic Stress Disorder Diagnostic Scale for Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition , Patient Health Questionnaire‐9, Generalized Anxiety Disorder‐7, Anxiety Sensitivity Index, Connor‐Davidson Resilience Scale, 36‐Item Short‐Form Health Survey, and an SCAD ‐specific questionnaire. Among 782 patients contacted, 512 surveys were returned. Most respondents were women (97.5%), with median age at time of SCAD and survey completion of 47 and 52 years, respectively. Eighty‐two percent had at least one trauma, with mild or more posttraumatic stress disorder symptoms in 28%. Symptoms of anxiety and depression were observed in 41% and 32%, respectively. On multivariable analysis, those of younger age at first SCAD and low resiliency scored higher on measures of trauma, anxiety, and depression. Those with higher anxiety sensitivity had more severe anxiety and posttraumatic stress disorder symptoms. Emotional and social quality of life was higher in those with high resiliency scores. Time from SCAD event to survey completion was associated with lower Generalized Anxiety Disorder‐7 score severity. Conclusions Survivors of SCAD have significant rates of posttraumatic stress disorder, depression, and anxiety, which are associated with lower quality of life specifically among those with lower resiliency. Given the prevalence and potential impact, screening and treatment for the psychological distress is advised. Behavioral interventions targeted toward resiliency training may be beneficial for this patient population.

Background Coronary artery disease risk factors are associated with atrial fibrillation ( AF ) and coronary endothelial dysfunction ( CED ). We hypothesized that CED is associated with increased risk of incident AF among patients with chest pain and nonobstructive coronary artery disease. Methods and Results Three hundred patients with chest pain, nonobstructive coronary artery disease, and no history of AF underwent intracoronary acetylcholine infusion for evaluation of baseline epicardial (decrease in mid–left anterior descending coronary artery diameter in response to acetylcholine) and microvascular (<50% increase in coronary blood flow in response to acetylcholine) CED . Primary outcome was incident AF over a mean follow‐up period of 10.5±5.5 years. Mean age was 53.3±10.8 years, and 70% were women. Baseline clinical and echocardiographic characteristics were similar between patients with CED (n=256) and those with normal endothelial function (n=44). Overall, 35 of 300 (12%) patients developed AF , among whom 34 of 35 (97%) had CED at baseline. Compared with normal endothelial function, the presence of CED was associated with 11% increased absolute risk and 5.8‐fold increased relative risk of incident AF . Moreover, CED ( odds ratio , 3.87; 95% CI , 1.27–47.0) and increased (>34 mL/m 2 ) left atrial volume index (odds ratio, 3.87; 95% CI , 1.60–9.11) were independent predictors of incident AF . Conclusions Patients with normal coronary endothelial function, as compared with those with CED and similar AF risk factors, have significantly lower incidence of AF on long‐term follow‐up. The potential mechanistic link between vascular dysfunction and AF development warrants further investigation.

Background: Type 2 myocardial infarction (T2MI) occurs because of an acute imbalance in myocardial oxygen supply and demand in the absence of atherothrombosis. Despite being frequently encountered in clinical practice, the population-based incidence and trends remain unknown, and the long-term outcomes are incompletely characterized. Methods: We prospectively recruited residents of Olmsted County, Minnesota, who experienced an event associated with a cardiac troponin T >99th percentile of a normal reference population (≥0.01 ng/mL) between January 1, 2003, and December 31, 2012. Events were retrospectively classified into type 1 myocardial infarction (T1MI, atherothombotic event), T2MI, or myocardial injury (troponin rise not meeting criteria for myocardial infarction [MI]) using the universal definition. Outcomes were long-term all-cause and cardiovascular mortality and recurrent MI. T2MI was further subclassified by the inciting event for supply/demand mismatch. Results: A total of 5460 patients had at least one cardiac troponin T ≥0.01 ng/mL; 1365 of these patients were classified as index T1MI (age, 68.5±14.8 years; 63% male) and 1054 were classified as T2MI (age, 73.7±15.8 years; 46% male). The annual incidence of T1MI decreased markedly from 202 to 84 per 100 000 persons between 2003 and 2012 ( P <0.001), whereas the incidence of T2MI declined from 130 to 78 per 100 000 persons ( P =0.02). In comparison with patients with T1MI, patients with T2MI had higher long-term all-cause mortality after adjustment for age and sex, driven by early and noncardiovascular death. Rates of cardiovascular death were similar after either type of MI (hazard ratio, 0.8 [95% CI, 0.7–1.0], P =0.11). Subclassification of T2MI by cause demonstrated a more favorable prognosis when the principal provoking mechanism was arrhythmia, in comparison with postoperative status, hypotension, anemia, and hypoxia. After index T2MI, the most common MI during follow-up was a recurrent T2MI, whereas the occurrence of a new T1MI was relatively rare (estimated rates at 5 years, 9.7% and 1.7%). Conclusions: There has been an evolution in the type of MI occurring in the community over a decade, with the incidence of T2MI now being similar to T1MI. Mortality after T2MI is higher and driven by early and noncardiovascular death. The provoking mechanism of supply/demand mismatch affects long-term survival. These findings underscore the healthcare burden of T2MI and provide benchmarks for clinical trial design.

Background: The clinical utility of routine electrocardiographic monitoring following percutaneous coronary interventions (PCI) is not well studied. Methods: We prospectively evaluated the incidence, cost, and the clinical implications of actionable arrhythmia alarms on telemetry monitoring following PCI. One thousand three hundred fifty-eight PCI procedures (989 [72.8%] for acute coronary syndrome and 369 [27.2%] for stable angina) on patients admitted to nonintensive care unit were identified and divided into 2 groups; group 1, patients with actionable alarms (AA) and group 2, patients with non-AA. AA included (1) ≥3 s electrical pause or asystole; (2) high-grade Mobitz type II atrioventricular block or complete heart block; (3) ventricular fibrillation; (4) ventricular tachycardia (>15 beats); (5) atrial fibrillation with rapid ventricular response; (6) supraventricular tachycardia (>15 beats). Primary outcomes were 30-day all-cause mortality. Cost-savings analysis was performed. Results: Incidence of AA was 2.2% (37/1672). Time from end of procedure to AA was 5.5 (0.5, 24.5) hours. Patients with AA were older, presented with acute congestive heart failure or non–ST-segment–elevation myocardial infarction, and had multivessel or left main disease. The 30-day all-cause mortality was significantly higher in patients with AA (6.5% versus 0.3% in non-AA [ P <0.001]). Applying the standardized costing approach and tailored monitoring per the American Heart Association guidelines lead to potential cost savings of $622 480.95 for the entire population. Conclusions: AA following PCI were infrequent but were associated with increase in 30-day mortality. Following American Heart Association guidelines for monitoring after PCI can lead to substantial cost saving.

Abstract Transradial angiography and intervention continues to become increasingly common as an access site for coronary procedures. Since the first “Best Practices” paper in 2013, ongoing trials have shed further light onto the safest and most efficient methods to perform these procedures. Specifically, this document comments on the use of ultrasound to facilitate radial access, the role of ulnar artery access, the utility of non‐invasive testing of collateral flow, strategies to prevent radial artery occlusion, radial access for primary PCI and topics that require further study.

Background: Mechanical injury in the conduction system requiring permanent pacemaker (PPM) associated with transcatheter aortic valve replacement (TAVR) procedure is a common complication. The objective of this study was to use ambulatory monitor BodyGuardian to assess late occurrence of atrioventricular block (AVB) after TAVR. Methods: This prospective study evaluated 365 patients who underwent TAVR at Mayo Clinic, Rochester, Minnesota between June 2016 and August 2017. Patients who received PPM for bradycardia after TAVR before discharge were considered as the PPM group. Those not requiring PPM received a BodyGuardian system (BodyGuardian group) for 30 days of continuous monitoring. Primary end point was Mobitz II or third-degree atrioventricular block (II/III AVB) at 30-day follow-up. Results: Of 365 patients, 74 who had a PPM or an implantable cardioverter-defibrillator before TAVR and 94 who were enrolled in other studies were excluded. Of 197 patients enrolled in the study, 70 (35.5%) received PPM and 127 had BodyGuardian before the hospital dismissal. Eleven of 127 (8.6%) BodyGuardian group required PPM within 30 days after TAVR for late occurrence of symptomatic bradycardia. In total, 33 of 197 (16.7%) patients developed II/III AVB (24 before and 9 after discharge). Thirty-four patients had preexisting right bundle branch block. Of them, 16 (47%) developed II/III AVB. Of 53 patients who developed new left bundle branch block after TAVR, 14% progressed to II/III AVB within 30 days. Conclusions: In patients without a standard post-TAVR pacing indication, yet a potential risk to develop AVB, a strategy of 30-day monitoring identifies additional patients who require permanent pacing.

Transradial access (TRA) is favored over transfemoral access for performing coronary angiography and percutaneous coronary intervention due to the reduced risk for vascular and bleeding complications and the documented survival benefit in ST-segment–elevation myocardial infarction patients who undergo primary percutaneous coronary intervention. TRA complications can be categorized as intra- or postprocedural and further categorized as related to bleeding or nonbleeding issues. Major intra- and postprocedural complications such as radial artery perforation and compartment syndrome are rare following TRA. Their occurrence, however, can be associated with morbid consequences, including requirement for surgical intervention if not identified and treated promptly. Nonbleeding complications such as radial artery spasm and radial artery occlusion are typically less morbid but occur much more frequently. Strategies to prevent TRA complications are essential and include the use of contemporary access techniques that limit arterial injury. This document summarizes contemporary techniques to prevent, identify, and manage TRA complications.

Background: We aim to study the incidence of major complications related to procedure defined as in-hospital death, myocardial infarction, stroke, pericardial effusion or tamponade, percutaneous coronary intervention due to iatrogenic coronary dissection, or unplanned bypass surgery within 72 hours after diagnostic left heart catheterization (LHC; primary end point). Furthermore, all causes of in-hospital death after LHC were adjudicated and reported (secondary end point). Methods and Results: Diagnostic LHC procedures (aortic angiography; coronary, including graft, angiography; and left ventricular angiography) from January 1, 2002, through December 31, 2013, were identified using the clinical scheduling system at Mayo Clinic, Rochester, and complications were identified through electronic records. International Classification of Diseases, Ninth Revision billing codes were used. Registration was queried to identify all-cause mortality. All events were reviewed and adjudicated. There were 43 786 diagnostic LHC procedures; 97.3% were coronary angiograms. The mean age of patients was 64.5 years (13.6), and the majority were male (61.5%). Primary end point was seen in 36 (0.082%) procedures or 8.2 of 10 000 LHCs. Combined right sided procedures with LHC did not increase the risk of major complications. Cardiogenic and septic shock, cardiac arrhythmia, and postsurgical complication were the most common causes of in-hospital death after LHC. Conclusions: The overall rates of major complications related to diagnostic cardiac catheterization procedures are extremely rare. The majority of the deaths occurring post-diagnostic LHC procedures were secondary to acute illness rather than directly related to diagnostic procedure.

Background: Spontaneous coronary artery dissection (SCAD) is an uncommon idiopathic disorder predominantly affecting young, otherwise healthy women. Rare familial cases reveal a genetic predisposition to disease. The aim of this study was to identify a novel susceptibility gene for SCAD. Methods: Whole-exome sequencing was performed in a family comprised of 3 affected individuals and filtered to identify rare, predicted deleterious, segregating variants. Immunohistochemical staining was used to evaluate protein expression of the identified candidate gene. The prevalence and spectrum of rare (<0.1%) variants within binding domains was determined by next-generation sequencing or denaturing high-performance liquid chromatography in a sporadic SCAD cohort of 675 unrelated individuals. Results: We identified a rare heterozygous missense variant within a highly conserved β-integrin–binding domain of TLN1 segregating with familial SCAD. TLN1 encodes talin 1—a large cytoplasmic protein of the integrin adhesion complex that links the actin cytoskeleton and extracellular matrix. Consistent with high mRNA expression in arterial tissues, robust immunohistochemical staining of talin 1 was demonstrated in coronary arteries. Nine additional rare heterozygous missense variants in TLN1 were identified in 10 sporadic cases. Incomplete penetrance, suggesting genetic or environmental modifiers of this episodic disorder, was evident in the familial case and 5 individuals with sporadic SCAD from whom parental DNA was available. Conclusions: Our findings reveal TLN1 as a disease-associated gene in familial and sporadic SCAD and, together with abnormal vascular phenotypes reported in animal models of talin 1 disruption, implicate impaired structural integrity of the coronary artery cytoskeleton in SCAD susceptibility.