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 Table of Contents  
REVIEW ARTICLE
Year : 2017  |  Volume : 1  |  Issue : 4  |  Page : 129-133

Bereavement: Relationship between grief and cardiovascular stress


De Gasperis Cardio Center, Niguarda Hospital, Milan, Italy

Date of Web Publication29-Oct-2018

Correspondence Address:
Dr. Alberto Roghi
Niguarda Hospital Piazza Ospedale Maggiore 3, 20162, Milan
Italy
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/hm.hm_5_18

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  Abstract 

It is well known that bereavement can cause ominous cardiovascular events and elicit aggressive behavior in bystanders. A multidisciplinary approach in end-of-life care including communication and taking into account cultural, social, emotional, religious, spiritual preferences, and local differences needs further development and implementation in health-care systems worldwide. The direct effects of emotional stress on the cardiovascular system and cardiac diseases most frequently implicated in sudden cardiac death are discussed.

Keywords: Bereavement, emotional stress, sudden cardiac death


How to cite this article:
Roghi A, Pedrotti P. Bereavement: Relationship between grief and cardiovascular stress. Heart Mind 2017;1:129-33

How to cite this URL:
Roghi A, Pedrotti P. Bereavement: Relationship between grief and cardiovascular stress. Heart Mind [serial online] 2017 [cited 2022 Aug 11];1:129-33. Available from: http://www.heartmindjournal.org/text.asp?2017/1/4/129/244373

A 51-year-old male collapsed suddenly at home while discussing with his wife at around midnight. The rescue team found him in ventricular fibrillation. Spontaneous circulation was restored after 14 min of cardiopulmonary resuscitation. A 12-lead electrocardiogram (ECG) showed sinus tachycardia with ST elevation in the anterior leads. Urgent coronary angiography at the nearest hospital showed occlusion of the left main coronary artery and critical ostial stenosis of the right coronary artery. The patient was transferred to our hospital for urgent surgical myocardial revascularization. Clinical condition was poor in spite of assisted mechanical ventilation and catecholamine infusion. The patient's wife witnessed rescue maneuvers but was not admitted on the ambulance. A neighbor gave her a ride to the hospital, but after a long search in the desert of the hospital's pavilions in the middle of the night, she found out that her husband had been transferred to our hospital for cardiac surgery. The neighbor had to leave, and after a desperate search, a friend was able to give her a ride to our hospital. She finally reached the intensive care unit where the cardiac surgeon was waiting for her. The communication was sharp and short: the patient was in critical conditions and survival chances were poor. The surgeon disappeared behind the sliding door while the woman collapsed on a chair in the corridor in front of the unit.

I was in charge of the coronary care unit, and the night had been very busy, so I was really disappointed by the last call from the emergency ward at dawn. The case was that of a middle-aged woman presenting with chest pain and diffuse ST elevation at 12-lead ECG. I was really astonished when I discovered that the patient I had been called for was the wife of the patient who had just died in our cardiac surgery operating theater. Urgent coronary angiography showed normal coronary arteries and left ventriculography showed severe impairment of left ventricular function, with apical ballooning. The following clinical course was uneventful, with progressive improvement of left ventricular function.


  Bringing Bad News and Bereavement Counseling Top


The relationship between emotional stress and the cardiovascular system is well known since the past. Heartbreak and broken heart are popular definitions of sudden cardiac death related to grief. The dangerous consequence of a superficial and unconscious bereavement is well known not only for the physical consequence related to the emotional stress but also even to the negative aggressive moods, sometimes elicited in the bystanders. Although the advance life support training courses have adopted since long time a dedicated chapter to bereavement,[1] the vast majority of health-care givers including physicians, nurses, and health technicians are generally shocked by the role playing generally adopted to train to bereavement. The common admission is that in their hospital, nobody takes care of that and bereavement is considered a question of individual empathy.

A multidisciplinary approach to the care at the end of life including communication, taking into account cultural, social, emotional, religious, spiritual preferences, and local differences needs further development and implementation in health-care systems worldwide. Compassionate communication with patients and loved ones is essential when dealing with end-of-life care. Privacy and adequate time are essential for good communication. Multidisciplinary bereavement programs are beneficial to families of patients who die in the emergency department. The grieving process may be supported by allowing unrestricted visiting, provision of clear verbal and written information, providing the opportunity to visit the deceased and facilitating religious procedures.

The direct effects of emotional stress on the cardiovascular system are summarized in the following subheadings, with a brief discussion about the state of the art of the relative physiopathology.


  Normal Cardiovascular Function Top


Emotional stress is driven to our brain by the peripheral sensitive apparatus eliciting a complex reflex including central and autonomic nervous systems with sympathovagal recruitment and adrenal stimulation with increasing catecholamine plasmatic concentration.[2] The final effect is rising of blood pressure, tachycardia, sweating, and peripheral vasoconstriction [Figure 1]. In a few people, a paradox effect due to the prevalence of vagal tone could prevail, inducing bradycardia, hypotension, gastrointestinal symptoms with nausea, diarrhea, and vomiting.
Figure 1: Relationship between stress, central, and peripheral nervous system stimulation and cardiovascular effects (Modified, Brotman DJ, Lancet 2007)

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  Takotsubo Syndrome Top


This syndrome is defined as a clinical condition mimicking acute coronary syndromes in which emotional stress precipitates chest pain, transitory ECG modifications, and typical left ventricular regional impairment. At angiography, coronary arteries are typically normal, and there is no or mild increase of markers of myocardial necrosis. Many different emotional stresses have been described in the literature since the first report published by Sato in 1990.[3] There is a prevalence in the female gender, with a good prognosis following the normalization of the ECG alterations and left ventricular impairment. The characteristic left ventricle apex ballooning mimicking the shape of the recipients used by Japanese fisherman to catch octopus (Takotsubo) is explained by catecholamine cardiotoxicity [Figure 2]. In the acute phase of Takotsubo, both epinephrine and norepinephrine released from adrenal medullar chromaffin cells are significantly increased with parallel increased stimulation of myocardial sympathetic nerve terminals. In the left ventricle, the β2 adrenoceptors are distributed with a gradient of increasing concentration between the base and the apex of the heart.[4] The different distribution along the left ventricle of β2 adrenoceptors is generally accepted to explain the different subtypes of left ventricular impairment described in the literature, with left ventricular apex ballooning largely prevalent. Epicardial and microvascular coronary spasm and increased cardiac workload are directly related to catecholamine toxicity, leading to the transitory myocardial damage.[5]
Figure 2: (a) Normal heart with left ventricular and aortic pressure. (b) Takotsubo heart with left ventricular apical ballooning due to catecholamine surge, 2 adrenoceptor apical distribution, coronary spasm (adapted from Akashi)

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  Coronary Artery Disease Top


Emotional stress is a well-known trigger of acute coronary syndromes. The increased sympathetic drive is generally considered a dangerous chronic condition in patients with occult or known coronary artery disease and is actively contrasted by beta-blocker therapy and training therapy. The deleterious effects of sympathetic and catecholamine stimulations over the cardiovascular system are related to multiple effects like the increase of myocardial oxygen consumption due to tachycardia and increased peripheral resistances, epicardial and microvascular vasoconstriction and spasm and the reduced threshold for supraventricular and ventricular arrhythmias. In patients with chronic coronary artery disease, a strong emotional stress can elicit angina, arrhythmias, congestive heart failure, and pulmonary edema. In patients at high risk for coronary artery disease, the so-called “vulnerable patients,” with multiple risk factors as metabolic syndrome, active smoke, hypertension, and diabetes, the emotional stress can elicit a catecholamine direct toxic effect on a vulnerable plaque in the coronary artery tree leading to vessel occlusion. The vulnerable plaque is generally a soft cholesterol plaque of the coronary artery wall. At the beginning of the atherosclerotic disease, the vessel remodeling increases wall thickness toward the external part of the artery, with no detrimental effect on coronary blood flow [Figure 3].[6] This explains why stress testing is not effective in the primary prevention of acute coronary syndromes. In the recent years, we gained significant improvement in the knowledge of vulnerable plaque. Before rupture, there is a significant thinning of the peripheral plaque cap, and in these conditions, weak triggers as the increase of sympathetic drive inducing tachycardia or increase in blood pressure could per se induce plaque disruption with platelets activation and vessel obstruction. Coronary spasm, microvascular disease, and concomitant inflammation have been recently suggested as significant triggers of acute coronary syndromes.[7]
Figure 3: Coronary flow is generally unaffected by vulnerable plaque, due to the external remodeling of epicardial vessels. Many factors, including emotional stress, are implicated in plaque rupture inducing abrupt vessel occlusion (adapted from Libby, Circulation 2001)

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  Hypertrophic Cardiomyopathy Top


Hypertrophic cardiomyopathy is a hereditable cardiac disease transmitted with an autosomal dominant trait caused by mutations in cardiac sarcomere protein genes, with a prevalence of 1 in 500 in the Caucasian population.[8] In the vast majority of cases, it is a benign disease with normal life expectancy, but in a minority of patients, it leads to severe progressive disease and heart failure. Sudden cardiac death is another ominous manifestation, particularly in young athletes. The physiopathology of sudden cardiac death in young athletes seems to be related to the sympathetic drive during exercise with lowering of arrhythmias threshold. In the subgroup of patients with the obstructive form of the disease, a dynamic intraventricular gradient is evident with increasing worsening during exercise or emotional stress. Early identification of subgroups of patients at high risk of sudden cardiac death is relevant to start appropriate lifestyle modifications and therapy. An integrated multidisciplinary approach including clinical, genetic, and imaging counseling is mandatory to properly assess high-risk patients.


  Ion Channel Disorders Top


Long QT syndrome (LQTS), Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia (CPVT) are inherited primary electrical disorders that predispose to sudden cardiac death in the absence of structural heart disease. The physiopathology of these disorders represents a model of the adverse interaction between adrenergic stimulation and ion channel dysfunction.[9]

The congenital LQTS is caused by mutations in several genes, all of which encode cardiac ion channels. The mutations identified in these genes produce either gain or loss of function, resulting in excess of late inward sodium current or in reduced outward potassium current (IKs). These ionic alterations lengthen action potential (AP) duration and explain the prolonged QT interval characteristic of LQTS. This situation favors the development of early afterdepolarizations, the trigger of ventricular arrhythmias. LQT1, accounting for >40% of all LQTSs, is caused by mutations in the KCNQ1 gene encoding the voltage-dependent K+ channel that mediates the slow component of the delayed rectifying IKs current. Since IKs currents respond to progressive adrenergic stimulation such as that present during exercise, LQT1 patients show a marked trend to present arrhythmia-related symptoms during sport practice as swimming. LQT2-related mutations entail a loss of function of KCNH2 with a consequent reduction in IKr, the rapid inflow potassium channel. Since IKr plays an important role in brisk increases in heart rate, LQT2 patients are prone to present arrhythmia-related symptoms in stress or emotional circumstances, as auditory stimuli.

LQT3 is caused by mutations in SCN5A encoding the voltage-dependent Na+ channel and mediator of the depolarizing INa current. Gain-of-function mutations in this gene, present in 10% of genetically diagnosed LQTS patients, prolong AP duration by increasing late depolarizing currents. In LQT3 patients, the defect in INa becomes more evident with slow heart rates, so it is common that these patients develop arrhythmia-related symptoms in circumstances of bradycardia and typically during sleep.[10] In LQT2 patients, emotion is the most important trigger of adverse cardiac events.[10]

The Brugada syndrome is characterized by a typical ECG pattern with a coved-type ST-segment elevation in the right precordial leads and a susceptibility to develop ventricular arrhythmias and sudden cardiac death.[11] From experimental studies, we know that the characteristic ECG pattern responds to an imbalance between inward and outward currents in the early phases of repolarization, created either by a decrease in inward or an increase in outward sodium currents. Mutation in 25 different genes has been described, and the molecular mechanisms proposed to explain the ECG pattern and arrhythmias are still object of debate. The final result of the ionic imbalance in early repolarization due to the malfunction of sodium channel currents is the epicardial and transmural dispersion of repolarization, favoring ventricular arrhythmias.

CPVT is a rare but extremely severe disease characterized by the presence of a normal ECG at baseline, but the predisposition to develop adrenergic-induced ventricular tachycardia that is typically bidirectional or polymorphic and can induce sudden cardiac death. Mechanistic studies have elucidated the molecular basis of CPVT, which relies on an abnormal release of Ca2+ from the sarcoplasmic reticulum in response to adrenergic stimulation. Excess Ca2+ is handled by the cell membrane Na+/Ca2+−exchanger, creating a net depolarizing current that can lead to arrhythmogenesis by a mechanism called delayed afterdepolarizations.[12] With an estimated prevalence of 1 in 10,000, CPVT is an inherited disorder with both autosomal dominant and recessive patterns of transmission. CPVT is usually an aggressive disorder, with symptoms likely appearing during childhood and a high incidence of cardiac events in follow-up. Due to the particular mechanism of this condition, arrhythmia-related symptoms such as syncope generally occur in adrenergically mediated circumstances such as exercise or emotional stress.


  Conclusions Top


The relationship between emotional stress and cardiovascular system is mediated by a complex interaction of peripheral and central nervous structures with neuroendocrine reflexes. The final effect is direct adrenergic cardiotoxicity inducing a wide range of different clinical pictures from the transitory impairment of left ventricular function to the more severe acute coronary syndromes or major ventricular arrhythmias responsible of sudden cardiac death.

The communication of bad news to an unknown person is always delicate, considering the risk related to the presence of hidden cardiac disease and different emotional reactivity in front of stress. In case of a patient with the known cardiac disease, in addition to the recommended modalities suggested, bereavement communication should be done with particular measures including mild sedation, family/friends cooperation, tailoring of cardiac therapy, and monitoring of vital parameters.



Extended knowledge of these interactions is necessary to improve the quality of communication of health givers.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Soar J, Nolan JP, Böttiger BW, Perkins GD, Lott C, Carli P, et al. European resuscitation council guidelines for resuscitation 2015: Section 3. Adult advanced life support. Resuscitation 2015;95:100-47.  Back to cited text no. 1
    
2.
Brotman DJ, Golden SH, Wittstein IS. The cardiovascular toll of stress. Lancet 2007;370:1089-100.  Back to cited text no. 2
    
3.
Sato H, Tateishi H, Uchida T, Dote K, Ishihara M. Tako-tsubo like left ventricular dysfunction due to multivessel coronary spasm. In: Clinical Aspect of Myocardial Injury. Tokyo: Kagakuhryononsha Publishing Co.; 1990. p. 56-64.  Back to cited text no. 3
    
4.
Akashi YJ, Nef HM, Lyon AR. Epidemiology and pathophysiology of Takotsubo syndrome. Nat Rev Cardiol 2015;12:387-97.  Back to cited text no. 4
    
5.
Pelliccia F, Kaski JC, Crea F, Camici PG. Pathophysiology of Takotsubo syndrome. Circulation 2017;135:2426-41.  Back to cited text no. 5
    
6.
Libby P. Current concepts of the pathogenesis of the acute coronary syndromes. Circulation 2001;104:365-72.  Back to cited text no. 6
    
7.
Crea F, Libby P. Acute coronary syndromes: The way forward from mechanisms to precision treatment. Circulation 2017;136:1155-66.  Back to cited text no. 7
    
8.
Authors/Task Force members, Elliott PM, Anastasakis A, Borger MA, Borggrefe M, Cecchi F, et al. 2014 ESC guidelines on diagnosis and management of hypertrophic cardiomyopathy: The Task Force for the Diagnosis and Management of Hypertrophic Cardiomyopathy of the European Society of Cardiology (ESC). Eur Heart J 2014;35:2733-79.  Back to cited text no. 8
    
9.
Garcia-Elias A, Benito B. Ion channel disorders and sudden cardiac death. Int J Mol Sci 2018;19. pii: E692.  Back to cited text no. 9
    
10.
Schwartz PJ, Priori SG, Spazzolini C, Moss AJ, Vincent GM, Napolitano C, et al. Genotype-phenotype correlation in the long-QT syndrome: Gene-specific triggers for life-threatening arrhythmias. Circulation 2001;103:89-95.  Back to cited text no. 10
    
11.
Brugada P, Brugada J. Right bundle branch block, persistent ST segment elevation and sudden cardiac death: A distinct clinical and electrocardiographic syndrome. A multicenter report. J Am Coll Cardiol 1992;20:1391-6.  Back to cited text no. 11
    
12.
Priori SG, Napolitano C, Memmi M, Colombi B, Drago F, Gasparini M, et al. Clinical and molecular characterization of patients with catecholaminergic polymorphic ventricular tachycardia. Circulation 2002;106:69-74.  Back to cited text no. 12
    


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