Spontaneous coronary artery dissection in old patients: clinical features, angiographic findings, management and outcome Free

Abstract

Introduction

Spontaneous coronary artery dissection (SCAD) is an uncommon cause of acute coronary syndrome (ACS). SCAD is defined as a spontaneous separation of the coronary artery wall layers that is not iatrogenic or related to trauma. It has been described as a young-to-middle aged people condition, predominantly affecting women.¹ The average age of women with SCAD ranges from 45 to 53 years, though young women can also be characteristically affected during pregnancy.² As a matter of fact, SCAD has been reported to be the first cause of acute myocardial infarction in pregnant women, yet less than 5% of women affected by SCAD are diagnosed during peripartum.³ Data from recent registries (mostly retrospective), as well as the universal access to coronary angiography in the setting of ACS, and the incremental use of intracoronary imaging techniques have altogether improved the knowledge about this disease. This new evidence provides a better understanding of the underlying pathophysiology of SCAD. Moreover, new imaging tools have been implemented by interventional cardiologists to confirm the diagnosis of SCAD in patients otherwise misdiagnosed.^4–7 All this information has led to the recent publication of two position papers by the European Society of Cardiology and the American Heart Association.^2,8 However, older patients constitute an interesting sub-population that is usually underrepresented in modern SCAD registries. To the best of our knowledge, clinical features, angiographic findings, management and outcomes in older patients with SCAD have not been previously described.

Methods

The prospective, nation-wide, Spanish Registry on SCAD (SR-SCAD) (NCT03607981) systematically included SCAD cases using specific case-report forms and predefined variables. A central Institutional Review Board approved the study for the entire country. From June 2015 to April 2019, 344 consecutive patients (387 lesions) from 31 academic Spanish centres were included. All coronary angiograms were carefully analysed jointly by two expert analysts (M.G.G. and F.A.) at a centralized corelab in the coordinator centre for predefined angiographic features. After careful revision, a total of 26 patients were excluded (3 patients withdrew informed consent; 4 had no coronary angiography of the index event; and 19 additional patients were excluded after angiographic review due to a high probability of an alternative diagnosis other than SCAD).

The present analysis includes prospectively collected data from 318 consecutive SCAD patients (358 lesions). Baseline demographic characteristics, personal history, data on admission, as well as events during hospitalization and at hospital discharge, were prospectively recorded. Data regarding angiographic findings as coronary artery location, morphological characteristics, number of affected vessels, as well as the type of treatment and results in those lesions treated by percutaneous coronary intervention (PCI), were also included.

Definitions

SCAD was defined as the acute development of a false lumen within the coronary artery wall not related to an atherosclerotic plaque, iatrogenic injury, or trauma. Angiographic SCAD patterns were categorized according to the previously described specific classification⁹ (Figure 1). Type 1 lesions were defined as those lesions with classic double lumen image. Type 2 lesions were defined as lesions that showed diffuse narrowing (>20 mm) without double-lumen, subclassifying them as Type 2a when the coronary artery recovered its normal caliber distally to the lesion and, 2 b when the lesion extends to the most distal segment of the vessel without recovery of the caliber. Type 3 lesions were defined as more focal stenosis (<20 mm) resembling atherosclerotic lesions. A fourth pattern (Type 4) was defined for lesions in which the first finding in angiography was an abrupt occlusion that does not allow its inclusion in any of the other patterns. Coronary tortuosity was analysed according to the method previously described by Eleid et al.,⁶ and classified as mild, moderate, or severe (Figure 2). Coronary artery ectasia was considered when a coronary segment was more than 1.5 times the diameter of an adjacent normal coronary segment¹⁰ (Figure 2). PCI success in SCAD was defined as flow improvement ≥1 in thrombolysis in myocardial infarction (TIMI) grade with a final TIMI 2–3 flow.

Figure 1

(A) Cranial coronary angiogram projection of a 72-year-old lady admitted by transient anterior ST-segment elevation myocardial infarction. Coronary angiogram depicts the presence of a long intramural haematoma (Type 2a lesion) involving mid-to-distal left anterior descending coronary artery (LAD) (delimited by white dashed lines). (B) Same projection at control coronary angiogram 6 months later, denoting the complete angiographic healing of the previous affected segment. (C) Right anterior oblique projection with caudal angulation in a 75-year-old lady admitted for non-ST-segment elevation myocardial infarction (NSTEMI). Coronary angiogram shows the presence of a Type 1 SCAD lesion (with typical double-lumen image) at a distal marginal branch (white asterisks) of the left circumflex coronary artery. (D) Control coronary angiogram 6 months later confirmed the complete angiographic healing of the segment affected by SCAD.

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Figure 2

Caudal (A) and cranial (B) coronary angiogram projections of a 70-year-old lady admitted by non-ST-segment elevation myocardial infarction (NSTEMI). Both projections denote severe coronary tortuosity as well as the presence of a long Type 2b intramural haematoma at the distal left anterior descending coronary artery (LAD) (yellow lines denote the beginning of the lesion at the distal LAD till the very distal segment of the coronary artery). Caudal (C) and spider (D) coronary angiogram projections of a 69-year-old lady admitted by NSTEMI. Proximal LAD showed an ectatic segment (white circle). At the left circumflex, a short intramural haematoma (Type 3 lesion) SCAD lesion can be visualized (white arrow).

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For the present analysis, SCAD patients were classified in two groups according to age; patients ≥65 years old were classified as older patients. Clinical and angiographic findings, management and in-hospital outcomes were compared between groups. A prespecified in-hospital major adverse cardiac event (MACE) was defined as the presence of death, myocardial reinfarction, unplanned coronary angiography or congestive heart failure during the index admission. Reinfarction was defined according to the Third Universal Definition of Myocardial Infarction.¹¹

Statistical analysis

Quantitative variables are presented as mean ± standard deviation or median [interquartile range (IQR)]. Categorical variables are presented as number (percentage). The Student’s t-test or the Mann–Whitney U were used to compare continuous variables. Pearson’s χ² test was used for categorical variables. A value of P < 0.05 was considered as statistically significant. All tests were performed with STATA 12 (StataCorp LLC, TX, USA).

Results

A total of 55 patients (17%) were ≥65 years old. Baseline characteristics and clinical presentation are summarized in Table 1. Median age in the older group was 71 years old and 51 in the younger one. In both groups, women represented more than 85% of patients included, with no significant differences between then. Older patients had more often hypertension (76% vs. 29%, P < 0.01) and dyslipidaemia (56% vs. 30%, P < 0.01), and less previous (4% vs. 18%, P < 0.001) or current (4% vs. 33%, P < 0.001) smoking habit. Previous history of ACS (including previous diagnosis of SCAD or myocardial infarction with non-obstructive coronary arteries—MINOCA) was more frequent in older patients (11% vs. 4%, P = 0.044). Supplementary material online, Table S1 includes the age at initial SCAD/MINOCA event and age at current SCAD event. We found no differences regarding other significant comorbidities or gynaecologic history. The most frequent clinical presentation in both groups was as non-ST-segment elevation myocardial infarction (62% vs. 52%, P = 0.172), followed by ST-segment elevation myocardial infarction (STEMI) (31% vs. 41%, P = 0.161), with no differences between groups. An identifiable trigger was more often found in young patients (43% vs. 27%, P = 0.028), being an emotional stressor the most commonly identified trigger in young patients (27% vs. 13%, P = 0.022). There were no differences between young and older SCAD patients in the median of time from symptoms onset to medical contact [120 min (IQR 60–300) vs. 125 min (IQR 40–464), P = 0.538] or from medical contact to coronary angiography [300 min (IQR 16–1696) vs. 397 (IQR 17–2220), P = 0.554].

Angiographic findings of the patients included are summarized in Table 2. There were no significant differences in the coronary artery affected by SCAD, as well as in the presence of multivessel or proximal involvement or initial TIMI flow. The left anterior descending coronary artery was the vessel most frequently affected by SCAD and Type 2a was the angiographic pattern most frequently found in both groups. Severe coronary tortuosity was more frequent in older SCAD patients (36% vs. 11%, P = 0.036). Similarly, coronary artery ectasia (24% vs. 9%, P < 0.01) was much more common in the older group.

Information on initial management and in-hospital outcomes is summarized in Table 3. Older patients were more often managed conservatively (89% vs. 75%, P = 0.025). In the older group, 6 patients (11%) were managed with PCI, all of whom presented with STEMI with initial TIMI flow 0–1. The remaining 11 patients over 65 with STEMI showed an initial TIMI flow 2–3 on coronary angiogram, thus initial management was conservative. Among those patients in whom an interventional strategy was planned, rate of PCI success was similar between groups (83% vs. 80%, P = 0.9). Both groups showed no significant differences regarding rise of biomarkers or the presence of left ventricular dysfunction. Besides, no differences were found in hospital length of stay. There were no significant differences between groups in the in-hospital MACE (7% vs. 8%, P = 0.858). Older patients showed a trend towards higher in-hospital mortality (3.6% vs. 0.8%, P = 0.082). Two patients in the older group died during admission. Both patients presented with anterior STEMI with refractory cardiogenic shock and finally died 4 and 7 days after admission. Regarding medical treatment at discharge, older patients significantly received less aspirin (83% vs. 94%, P < 0.01). The prescription of dual antiplatelet therapy (DAPT) was similar in both groups (53% vs. 60%, P = 0.340) and there was a non-significant trend towards a higher prescription of oral anticoagulation in the older group (13% vs. 6%, P = 0.062). Patients over 65 years of age received more often angiotensin-converting enzyme inhibitors or angiotensin receptor blockers (72% vs. 47%, P < 0.01) and statins (91% vs. 77%, P = 0.023).

Discussion

To the best of our knowledge, this is the first study addressing clinical features, angiographic findings, management and in-hospital outcomes in older patients with SCAD. We found that older patients with SCAD had more often cardiovascular risk factors such as hypertension and dyslipidaemia, as well as previous history of ACS (including previous SCAD or MINOCA). In addition, compared with younger patients, they showed more severe coronary artery tortuosity and coronary artery ectasia on angiography. This elderly group was more often managed conservatively, and had similar short-term outcomes compared with those in younger patients.

SCAD has been classically considered a disease of young women. However, recent series have demonstrated that most patients are middle aged, and this condition has also been reported in old patients. No previous study has focused on the characteristics of SCAD in this specific age-group population.^1,9,12 In our study, patients were classified into two groups according to age ≥65 or <65. Median age in the older group was 71 years old, while it was 51 in the younger one, the latter similar to that observed in large contemporary registries.^7,9,12,13 Our findings underscore that the diagnosis of SCAD should also be considered in older patients. Furthermore, 5% of the global cohort had a previous diagnosis of ACS, that included both a previous SCAD event or an episode of MINOCA (in most cases probably a misdiagnosed SCAD event). The diagnosis of previous ACS was more frequent in older patients. Interestingly, it seems that the risk of recurrence in SCAD does not vanish at older ages, suggesting that long-term surveillance of SCAD survivors is necessary, as young patients with SCAD might develop late recurrences on follow-up.

It has been reported that SCAD patients usually have fewer traditional cardiovascular risk factors than patients with atherosclerotic coronary artery disease (CAD)..¹² However, in the subset of older patients, we observed a higher prevalence of hypertension and dyslipidaemia, as well as previous history of ACS than those under 65. All such findings may be related to age itself. Previous observational data showed that hypertension seems to be related to a higher risk of recurrences in SCAD.¹⁴ Furthermore, older patients with SCAD might have been misdiagnosed as conventional atherosclerotic CAD at a previous event, the first recognized SCAD event being more probably a recurrence of SCAD. Our data seem to demonstrate that older SCAD patients have some specific characteristics compared with younger patients. This may only reflect dynamic changes over time within the same condition rather than an interaction between atherosclerotic CAD and SCAD.

Current evidence supports conservative management in most patients with SCAD.^2,8 This approach is based on observational data showing that a high proportion of SCAD lesions completely heal at late follow-up. Furthermore, PCI results in SCAD are suboptimal, entailing a higher risk of complications, especially when compared with atherosclerotic CAD.^7,15 Accordingly, an invasive approach with PCI is only recommended in the setting of ongoing or recurrent ischaemia, haemodynamic or electrical instability or left main involvement.^2,16–18 Despite no differences between the two groups regarding clinical presentation, anatomical distribution of SCAD lesions and initial TIMI flow, in our study, older patients were more often managed conservatively than younger patients. In this regard, older patients with SCAD had more tortuous coronary arteries, a finding that may have influenced decision-making, with operators avoiding PCI in more tortuous coronary segments that could lead to a potential increase in PCI failure or complications. However, the low number of hard in-hospital adverse events does not allow us to confirm whether less access to coronary revascularization techniques is associated with a worse prognosis in older patients with SCAD. In this regard, despite the existing differences in the initial strategy selected, we found no differences in in-hospital outcomes between groups.

Antithrombotic therapy after SCAD remains challenging, especially in older patients. Patients with SCAD who undergo coronary revascularization should receive the standard guideline-based DAPT.¹⁹ Evidence of antithrombotic therapy in the setting of conservative management is still lacking. However, most experts recommend at least 1 year of aspirin therapy. The use of DAPT should be based on a personalized approach balancing individual ischaemic and bleeding risks.² So far, short or long-term ischaemic and bleeding outcomes related to the use of DAPT or aspirin alone in SCAD have not been evaluated.² Although only 11% of the older patients in our study were treated with PCI, more than 50% of them were discharged with DAPT, which is consistent with previous registries but reflects the lack of a systematic therapeutic approach and the need for further data from larger prospective cohorts of patients with this condition.

Our study has some limitations that merit discussion. First of all, it is an observational study so we cannot rule out the possibility of selection bias. Secondly, although participating centres enrolled consecutive patients with SCAD, we cannot rule out misdiagnosis of a number of cases. Moreover, although overlooking the diagnosis of SCAD may occur at any age, this problem may be more relevant in older patients in whom the clinical suspicious of SCAD may be low. Third, despite the absence of signs of significant angiographic coronary atherosclerosis in older patients with SCAD, we cannot completely exclude the possibility of underlying atherosclerosis as a promoting factor to dissection in some of these older patients. Fourth, the lack of evidence-based algorithms for SCAD favours heterogeneity in acute management between centres. In spite of these limitations, we think that this nationwide study provides new and interesting information about SCAD in older patients from a large prospective cohort of consecutive unselected SCAD patients.

In conclusion, older patients with SCAD show differences in clinical background and angiographic findings compared with young SCAD patients. Initial management differs between groups, with older patients being more often managed conservatively. However, in-hospital composite outcomes were low, and not different from those seen in younger SCAD patients.

Supplementary material

Supplementary material is available at European Heart Journal: Acute Cardiovascular Care online.

Conflict of interest: none declared.

Consent: Written informed consent for patient information and images to be published was provided by the patient(s) or a legally authorized representative.

References

Author notes