Impact of paramedic education on door-to-balloon times and appropriate use of the primary PCI pathway in ST-elevation myocardial infarction.

OBJECTIVE: Evidence supports improved outcomes and reduced mortality with rapid reperfusion through primary percutaneous coronary intervention (PPCI) for ST-elevation myocardial infarction (STEMI). UK national audit data (Myocardial Ischaemia National Audit Project [MINAP]) demonstrates minor improvements in door-to-balloon times (DTB) of <90 min but increasing call-to-balloon times (CTB). We evaluate the effect of a regional Cardiologist delivered paramedic education programme (PEP) on DTB times and appropriate use of the PPCI pathway. METHODS: This was a prospective single-centre study of patients with STEMI brought directly to hospital via ambulance services. Data sources included ambulance charts, in-patient notes, British Cardiovascular Interventional Society (BCIS) database and local MINAP data. All DTB breaches were investigated. A local PEP was implemented with focus on ECG interpretation, STEMI diagnosis and appropriate use of the PPCI pathway. Non-parametric Wilcoxon rank test was used for comparisons of DTB and CTB times between direct versus ED-associated cath lab transfer. RESULTS: A total of 728 patients with STEMI were admitted directly to our centre via ambulance, 66% (n=484) directly to the Catheterisation Laboratory (Cath Lab) and 34% (n=244) via the Emergency Department (ED). There was a significant increase in median DTB, 83 vs 37 min (p<0.001) and median CTB 144 vs 97.5 min (p<0.001) when transfer to the Cath Lab occurred via the ED versus direct transfer. The PEP increased direct cath lab transfers (52%-85%) and generated annual reductions in median DTB times, with sustained improvement seen throughout the 7-year study period. CONCLUSIONS: Paramedic education increases direct transfer of STEMI patients to the Cath Lab, and reduces DTB times. This is an effective and reproducible intervention to facilitate timely reperfusion in STEMI.

Outcome of left main stem percutaneous coronary intervention in a UK nonsurgical center: A 5-year clinical experience.

OBJECTIVES: To evaluate the outcome of unprotected left main stem (LMS) percutaneous coronary intervention (PCI) in a large UK nonsurgical center. BACKGROUND: PCI on unprotected LMS is increasingly regarded as a viable alternative to coronary artery bypass grafting (CABG) with comparable outcome and safety profile in select groups. The safety and efficacy of unprotected LMS PCI without on-site surgical back up has not been reported. METHODS: Data on all unprotected LMS PCI performed between January 2011 and December 2015, was collected from the local PCI database and electronic patient records. In hospital and 1-year major adverse cardiovascular events (MACE) (all-cause mortality, myocardial infarction [MI], stroke, and target vessel revascularization [TVR]) was recorded. RESULTS: 249 patients had unprotected LMS intervention during the study period. 77% of patients (n = 192) were male and mean age was 70 ± 12 years. 31% (n = 78) of cases were elective, 44% (n = 109) NSTEMI, and 25% (n = 62) STEMI. Anatomical distribution: 19% (n = 47) ostial left main, 31% (n = 77) shaft, and 50% (n = 125) bifurcation. The mean SYNTAX score was 24.4 ± 10.6. 22% (n = 55) of patients had severe LV impairment preprocedure and 13% (n = 33) were in cardiogenic shock at presentation. 35% (14%) required IABP support. The vast majority (98.4%) of procedures were successful. No patients required emergency transfer for CABG surgery. There were 25 (10%) in-hospital deaths. 68% of in-hospital deaths occurred in patients undergoing primary PCI for STEMI. 72% of patients who died were in cardiogenic shock at presentation. The 12-month MACE rate was 17.2%. Death occurred in 11.6%, MI in 2.4%, TVR in 2.4%, and stroke in 0.8% of patients. CONCLUSION: These results highlight the safety and efficacy of unprotected LMS PCI in a high volume non-surgical center.

Hostility and physiological responses to laboratory stress in acute coronary syndrome patients.

OBJECTIVE: Evidence suggests that emotional stress can trigger acute coronary syndromes in patients with advanced coronary artery disease (CAD), although the mechanisms involved remain unclear. Hostility is associated with heightened reactivity to stress in healthy individuals, and with an elevated risk of adverse cardiac events in CAD patients. This study set out to test whether hostile individuals with advanced CAD were also more stress responsive. METHODS: Thirty-four men (aged 55.9+/-9.3 years) who had recently survived an acute coronary syndrome took part in laboratory testing. Trait hostility was assessed by the Cook Medley Hostility Scale, and cardiovascular activity, salivary cortisol, and plasma concentrations of interleukin-6 were assessed at baseline, during performance of two mental tasks, and during a 2-h recovery. RESULTS: Participants with higher hostility scores had heightened systolic and diastolic blood pressure (BP) reactivity to tasks (both P<.05), as well as a more sustained increase in systolic BP at 2 h post-task (P=.024), independent of age, BMI, smoking status, medication, and baseline BP. Hostility was also associated with elevated plasma interleukin-6 (IL-6) levels at 75 min (P=.023) and 2 h (P=.016) poststress and was negatively correlated with salivary cortisol at 75 min (P=.034). CONCLUSION: Hostile individuals with advanced cardiovascular disease may be particularly susceptible to stress-induced increases in sympathetic activity and inflammation. These mechanisms may contribute to an elevated risk of emotionally triggered cardiac events in such patients.

Pre-hospital delay in patients with acute coronary syndrome: factors associated with patient decision time and home-to-hospital delay.

BACKGROUND: Pre-hospital delays in patients experiencing acute coronary syndromes (ACS) remain unacceptably long. AIMS: To examine simultaneously a wide range of clinical, sociodemographic and situational factors associated with total pre-hospital delay and its two components. METHODS: Pre-hospital delay data were collected from 228 patients with ACS using patient's medical notes and semi-structured interviews. Total pre-hospital delay (symptom onset to hospital admission) was divided into 2 components: decision time (symptom onset to call for medical help), and home-to-hospital delay (call for help to hospital admission). RESULTS: Shorter total pre-hospital delays and decision times were associated with ST segment myocardial infarction (STEMI), recognizing symptoms as cardiac in origin, being married, symptom onset outside the home and the presence of a bystander. Shorter home-to-hospital delays were more likely among younger patients, those experiencing an STEMI, and patients reporting a greater number of symptoms. Initial contact with emergency medical services was related to shorter total delays and decision times. CONCLUSIONS: Different factors were associated with shorter times in the 2 component phases. Greater understanding of the factors impacting on the component phases may help target interventions more effectively and reduce pre-hospital delays.

Practical support predicts medication adherence and attendance at cardiac rehabilitation following acute coronary syndrome.

OBJECTIVE: Poor social support is associated with recurrent cardiac events following acute coronary syndrome (ACS). Interventions have largely targeted emotional support, but practical support may be particularly important in encouraging recovery behaviors. We assessed whether practical and emotional support differentially predicted medication adherence and rehabilitation attendance following ACS. METHODS: This prospective observational clinical cohort study involved 262 survivors of verified ACS, recruited from four coronary care units in the London area. Practical and emotional support were measured in hospital, and depression, 7-10 days after discharge. Medication adherence and rehabilitation attendance were assessed by telephone interview 12 months after hospitalization. RESULTS: Nearly one third of patients (29.8%) had no practical supports, 16% had one, and 54.2% had two or more sources of practical support. Patients with greater practical support were more likely to adhere to medication (P=.034) independently of age, gender, marital status, clinical risk profile, and depression. There was also an association with rehabilitation attendance (P=.034), but this was no longer significant after depression had been taken into account. Emotional support was unrelated to medication adherence and rehabilitation attendance. CONCLUSIONS: Cardiac patients with greater practical support may receive more prompts about medications, help with filling prescriptions and assistance with cardiac rehabilitation attendance. These behaviors can influence long-term recovery.

Causal beliefs, cardiac denial and pre-hospital delays following the onset of acute coronary syndromes.

Reducing pre-hospital delay is crucial in reducing mortality from acute coronary syndrome (ACS). Patient's causal beliefs and coping styles may affect symptom appraisal and help-seeking behavior. We examined whether patient's beliefs about the causes of their ACS and denial of impact were associated with pre-hospital delay. Pre-hospital delay data were collected from 177 patients with ACS. Retrospective causal beliefs and cardiac denial of impact were assessed using questionnaires. Factor analysis of causal beliefs produced 3 factors; beliefs in stress and emotional state, behavioral and clinical risk factors, and in heredity as causal influences. Patients with strong beliefs that stress and emotional state caused their ACS were more likely to have long pre-hospital delays (>130 min). There were no significant associations between pre-hospital delay and the other two causal belief factors. Patients with greater denial scores were also more likely to have long delays than those with low scores. These effects were independent of age, gender, education, previous myocardial infarction, history of depression and negative affectivity. Cognitive and emotional factors including patient's beliefs about causes and avoidant coping help to explain variations in pre-hospital delay.

Type-D personality and cortisol in survivors of acute coronary syndrome.

OBJECTIVE: To test the hypothesis that Type-D personality is associated with elevated cortisol levels in patients 4 months after an acute coronary syndrome (ACS). METHODS: Salivary cortisol profiles were measured at home in 70 coronary heart disease patients (Mean age = 60.90 years, SD = 10.7, 17% female) 4 months after hospitalization for ACS. Eight saliva samples were taken over the course of 1 day. RESULTS: Thirty eight percent of the ACS patients were defined as Type-D. Cortisol profiles showed a typical diurnal pattern, with low levels in the evening, high levels early in the day. Type-D was not related to the cortisol awakening response, but cortisol output the day was higher in Type-D (mean = 4443.3, SD = 2334.1 nmol/l) than non Type-D patients (mean = 3252.0, SD = 1810.2 nmol/l) after adjustment for age, gender, hypertension, Global Registry of Acute Coronary Events risk score, recurrence of cardiac symptoms, previous myocardial infarction, body mass index and concurrent depressed mood (p = .044). Type-D personality accounted for 6% over the variance in cortisol output over the day, after covariates had been taken into account. CONCLUSION: Type-D personality may be associated with prolonged disruption of the hypothalamic-pituitary-adrenal axis function in survivors of acute cardiac events and may contribute to biological responses influencing future cardiac morbidity.

Social networks and partner stress as predictors of adherence to medication, rehabilitation attendance, and quality of life following acute coronary syndrome.

OBJECTIVE: This study examined whether social network size and partner stress predicted medication adherence, cardiac rehabilitation attendance, and quality of life 12 months following hospitalization for an acute coronary syndrome (ACS). DESIGN: ACS patients (N = 193, M age = 60.6 years, SD = 11.4 years, 23% female) were recruited shortly following admission to 4 local hospitals. A prospective design was employed with follow-up data collected 12 months following hospital admission. MAIN OUTCOME MEASURES: Data were gathered on social network size and partner stress. The main outcomes assessed at 12 months were medication adherence, cardiac rehabilitation attendance, and quality of life (Short Form 36). RESULTS: Partner stress predicted medication nonadherence, odds ratio: 2.89, (95% CI = 1.21, 6.95). ACS patients with large social networks were more likely to attend rehabilitation, odds ratio: 3.42, (95% CI = 1.42, 8.25). Analyses were adjusted for age, gender, clinical risk scores, readmission/recurrence, and negative affectivity. Both partner stress and smaller social network size were associated with poorer quality of life. CONCLUSION: Social network size and partner stress may partly exert their influence on coronary heart disease morbidity and mortality through recovery behaviors and maintenance of quality of life.

Cortisol awakening response is elevated in acute coronary syndrome patients with type-D personality.

OBJECTIVE: Type-D or "distressed" personality and depression following admission for acute coronary syndrome (ACS) have been associated with poor clinical outcome. The biological pathways underpinning this relationship may include disruption of the hypothalamic-pituitary-adrenocortical (HPA) axis. We therefore assessed cortisol output in patients who had recently suffered from ACS. METHOD: Salivary cortisol was assessed eight times over a 24-h period in 72 patients within 5 days of admission for ACS. Depressive symptoms were measured with the Beck Depression Inventory (BDI), and type-D personality was measured with the Type-D Scale-16. Particular attention was given to cortisol awakening response (CAR), which was measured as the difference in cortisol between waking and peak responses 15-30 min later. RESULTS: Cortisol showed a typical diurnal pattern, with low levels in the evening, high levels early in the day, and CAR averaging 7.58+/-10.0 nmol/l. Cortisol was not related to the severity of ACS or underlying coronary artery disease or to BDI scores. The CAR was positively associated with type-D personality independently of age, gender, and body mass (P=.007). Linear regression showed that type-D personality accounted for 7.9% of the variance in CAR after age, sex, body mass, BDI, cortisol level on waking, and fatigue had been taken into account (P=.008). CONCLUSIONS: Type-D personality may be associated with disruption of HPA axis function in survivors of acute cardiac events and may contribute to heightened inflammatory responses influencing future cardiac morbidity.

Acute depressed mood as a trigger of acute coronary syndromes.

BACKGROUND: Some cases of acute coronary syndrome (ACS) may be triggered by emotional states such as anger, but it is not known if acute depressed mood can act as a trigger. METHODS: 295 men and women with a verified ACS were studied. Depressed mood in the two hours before ACS symptom onset was compared with the same period 24 hours earlier (pair-matched analysis), and with usual levels of depressed mood, using case-crossover methods. RESULTS: 46 (18.2%) patients experienced depressed mood in the two hours before ACS onset. The odds of ACS following depressed mood were 2.50 (95% confidence intervals 1.05 to 6.56) in the pair-matched analysis, while the relative risk of ACS onset following depressed mood was 4.33 (95% confidence intervals 3.39 to 6.11) compared with usual levels of depressed mood. Depressed mood preceding ACS onset was more common in lower income patients (p = .032), and was associated with recent life stress, but was not related to psychiatric status. CONCLUSIONS: Acute depressed mood may elicit biological responses that contribute to ACS, including vascular endothelial dysfunction, inflammatory cytokine release and platelet activation. Acute depressed mood may trigger potentially life-threatening cardiac events.

Pathophysiological processes underlying emotional triggering of acute cardiac events.

Acute negative emotional states may act as triggers of acute coronary syndrome (ACS), but the biological mechanisms involved are not known. Heightened platelet activation and hemodynamic shear stress provoked by acute stress may contribute. Here we investigated whether patients whose ACS had been preceded by acute anger, stress, or depression would show heightened hemodynamic and platelet activation in response to psychophysiological stress testing. We studied 34 male patients an average of 15 months after they had survived a documented ACS. According to an interview conducted within 5 days of hospital admission, 14 men had experienced acute negative emotion in the 2 h before symptom onset, and 20 men had not experienced any negative emotion. Hemodynamic variables and platelet activation were monitored during performance of challenging color-word interference and public speaking tasks and over a 2-h poststress recovery period. The emotion trigger group showed significantly greater increases in monocyte-platelet, leukocyte-platelet, and neutrophil-platelet aggregate responses to stress than the nontrigger group, after adjusting for age, body mass, smoking status, and medication. Monocyte-platelet aggregates remained elevated for 30 min after stress in the emotion trigger group. The emotion trigger group also showed poststress delayed recovery of systolic pressure and cardiac output compared with the nontrigger group. These results suggest that some patients with coronary artery disease may be particularly susceptible to emotional triggering of ACS because of heightened platelet activation in response to psychological stress, coupled with impaired hemodynamic poststress recovery.

Frequency of distress and fear of dying during acute coronary syndromes and consequences for adaptation.

Experiencing an acute coronary syndrome (ACS) may provoke a range of negative emotional responses, including acute distress and fear of dying. The frequency of these emotional states has rarely been assessed. This study examined the presence and severity of the fear of dying and acute distress in 184 patients with ACS and analyzed its correlates and consequences. Intense distress and fear of dying was reported by 40 patients (21.7%) and moderate fear and distress by 95 patients (51.6%). Intense distress and fear was associated with female gender (odds ratio [OR] 2.49, 95% confidence interval [CI] 1.07 to 2.49), lower levels of education (OR 2.44, 95% CI 1.02 to 5.87), greater chest pain (OR 5.33, 95% CI 1.40 to 20.4), and emotional upset in the 2 hours before onset of ACS (OR 2.70, 95% CI 1.13 to 6.45). Having no acute distress or fear was more common in patients who exercised regularly (OR 3.32, 95% CI 1.35 to 8.18) and who did not initially attribute the chest pain to cardiac causes (OR 2.67, 95% CI 1.10 to 6.47). No association was found with cardiovascular disease history, objective measures of clinical severity, or with clinical presentation of ACS. Acute distress and fear of dying predicted greater depression and anxiety 1 week after ACS (p=0.006), and elevated levels of depression at 3 months (p=0.009), after adjustment for age, gender, and negative affect. In conclusion, distress and fear during the initial stages of an ACS may trigger subsequent depression and anxiety, thereby promoting poorer prognosis and greater morbidity with time.

Behavioral and emotional triggers of acute coronary syndromes: a systematic review and critique.

OBJECTIVE: The objective of this study was to review the evidence that behavioral and emotional factors are triggers of acute coronary syndromes. METHOD: Systematic review of the published literature from 1970 to 2004 of trigger events, defined as stimuli or activities occurring within 24 hours of the onset of acute coronary syndromes. RESULTS: There is consistent evidence that physical exertion (particularly by people who are not normally active), emotional stress, anger, and extreme excitement can trigger acute myocardial infarction and sudden cardiac death in susceptible individuals. Many triggers operate within 1 to 2 hours of symptom onset. There are methodologic limitations to the current literature, including sampling, retrospective reporting, and presentation biases, the role of memory decay and salience, and reverse causation because of silent prodromal events. CONCLUSIONS: Behavioral and emotional factors are probable triggers of acute coronary syndromes in vulnerable individuals, and the pathophysiological processes elicited by these stimuli are being increasingly understood. The benefits to patients of knowledge to these processes have yet to accrue.

Mild acute inflammatory stimulation induces transient negative mood.

OBJECTIVE: This study aims to assess the mood changes induced by mild acute inflammatory stimulation (typhoid vaccination). METHODS: Using a double blind study design, 26 healthy volunteers underwent baseline assessments of mood, financial strain and work stress and were randomised to injection of Salmonella typhi vaccine or placebo injection. Mood, symptoms and body temperature was assessed by a modified version of the Profile of Mood States at 1, 2, 3, 4, 6 and 8 h post injection. RESULTS: Typhoid vaccination induces no increases in physical symptoms or temperature. Mood improved over the day in the placebo but not in the vaccine condition. Negative changes in mood following injection were correlated with chronic stress (financial strain) in the vaccination condition (r=-.65, P<.025). CONCLUSION: A mild acute inflammatory stimulus induces transient negative mood, and responses were modulated by chronic stress. Implications for depressed mood in physical illness are discussed.

Exaggerated platelet and hemodynamic reactivity to mental stress in men with coronary artery disease.

OBJECTIVE: This study compared the effects of acute mental stress on cardiovascular and subjective responses and platelet activation in male patients with established coronary artery disease (CAD) and age-matched controls. METHODS: We assessed 17 male CAD patients aged 44 to 59 years and 22 healthy male controls. Blood pressure, heart rate, and hemodynamics were assessed before, during, and up to 2 hours after administration of color/word and mirror tracing tasks. Blood was sampled at baseline, after tasks, and at 30 and 75 minutes after stress, and platelet activation was assessed by measuring platelet-leukocyte aggregates (PLAs) using flow cytometry. RESULTS: CAD patients showed significantly greater systolic blood pressure stress responses than controls (mean increases of 43.9 and 28.3 mm Hg, adjusted for income, body mass index, waist/hip ratio, and medication), together with larger increases in heart rate (14.1 and 4.7 bpm) and cardiac index. Total peripheral resistance increased during the poststress recovery period in CAD patients but not in controls. PLAs increased with stress in both groups, but remained elevated at 75 minutes in CAD patients, returning to baseline in controls. Heart rate and cardiac index responses were correlated with increases in subjective stress and with depression ratings, whereas PLA responses were associated with ratings of task difficulty. CONCLUSION: Acute mental stress stimulated heightened cardiovascular responses in CAD patients, coupled with more prolonged platelet activation. These factors may contribute to plaque rupture and thrombogenesis, and partly mediate stress-induced triggering of acute coronary syndromes.

Psychosocial factors in the development of coronary artery disease.

The fact that traditional risk factors only account for approximately two thirds of cases of coronary artery disease (CAD) has stimulated increasing interest in the relationship between CAD and psychosocial factors. Five areas--chronic stress, socioeconomic status (SES), personality, depression, and social support--have been most thoroughly examined. There is evidence to support a causal relationship between chronic stress, SES, depression, and social support and development of CAD. In this article, we discuss the epidemiologic evidence linking psychosocial factors and CAD, and review the effects of psychosocial factors on several pathophysiologic mechanisms that have been proposed as potential mediators of CAD. The hypothalamic-pituitary-adrenal axis, hypertension and cardiovascular reactivity, endothelial function, inflammatory markers, platelets, coagulation factors, fibrinogen, lipids, glucose metabolism, and lifestyle factors have all been implicated in this process. Recently, the first intervention trials have been carried out, although with initially disappointing results. Reducing the cardiovascular risk due to these psychosocial factors will be one of the major health care challenges in the future.

New insights into the mechanisms of temporal variation in the incidence of acute coronary syndromes.

Over the last few years, patterns have emerged regarding the daily (circadian), weekly (circaseptan), and yearly (circannual) variation in the incidence of acute coronary syndromes (ACS). Peaks of incidence occur in the morning, on Mondays, and in winter. There is a difference in the pattern of incidence in different subgroups such as diabetics and smokers, which, along with the incidence alteration seen with aspirin and beta blockers, gives us some potential understanding of underlying mechanisms. Recent advances in the study of endothelial function, cytokine biology, and adhesion molecules have led to new insights into the way that natural fluctuations in these systems may affect ACS incidence. It is hoped that understanding these developments will lead to therapeutic advances in ACS prevention.