Pain in the heart area - types of problems that have this symptom

Causes of heart pain

Acute aching pain in the heart area occurs in a person regardless of age, conditions and circumstances. However, not every one of them may indicate heart problems. Depending on the mechanism of formation, all chest pains can be divided into cardiac and non-cardiac etiologies.

Stitching pain in the heart area can occur for various reasons, with diseases of other organs with irradiation of the pain syndrome into the chest.

Diseases of the neuromuscular system:
Pain in the cervical spine;
Myalgia;
Intercostal neuralgia.
Pathologies of large vessels:
Pulmonary embolism.
For pathology of the digestive system:
Pancreas;
Esophagus;
Gallbladder.
Diseases of the respiratory system:
Pneumothorax;
Pneumonia;
Pleurisy;
Tuberculosis.
Nervous system diseases:
Panic attacks.
Diseases of viral etiology:

If, with pain in the heart area, there is pressure and radiates to the left hand and little finger, this may result in angina pectoris. Acute pain syndrome develops with myocardial infarction, dull pain characterizes chronic ischemic heart disease.

Depression, anxiety and cardiovascular health

Among patients with cardiovascular diseases, the incidence of concomitant depression is 22–33% [1–4]. Depression may also be considered a risk factor for the development of cardiac disease [5–8]. Therefore, it is appropriate to more thoroughly investigate the association of depression and anxiety with cardiovascular disease, as well as the pathophysiological mechanisms underlying this relationship. This will improve the effectiveness of treatment and possibly improve the prognosis.

Link between depression and anxiety and cardiovascular disease

Classic epidemiological principles can be used to assess the extent to which depression and anxiety are associated with cardiovascular disease. The main criteria used for such an assessment are the strength of the connection, the presence of a dose-dependent relationship, and the sequence of combination. Some of the studies examining the association between cardiovascular disease and depression are relatively well-controlled, prospective in design, use structured clinical interviews as a diagnostic tool, control for other risk factors for CAD, and control for demographic factors [6–15]. According to these studies, the relative risk of having major depression or depressive symptoms for progression to cardiovascular disease or cardiovascular mortality ranges from 1.5 to 4.5. These rates, which are quite high for epidemiological studies, demonstrate a fairly strong association between depression and CHD.

There are no studies yet that show that patients with more severe depression also have more severe cardiovascular disease. The extremely small number of prospective studies does not allow us to establish whether ischemic heart disease actually occurs more often in patients who were initially depressed but had no signs of cardiovascular disease. There is no evidence yet that adequate treatment of depression leads to a reduction in subsequent cardiac events. Two studies: ENRICHO (Enhanced Recovery in Coronary Heart Disease) and SADHART (Sertralin Antidepressant Heart Attack Recovery Trial), which are currently underway, should yield results in the near future.

At the same time, it has been shown that patients with higher levels of anxiety develop more severe forms of coronary artery disease. Kawachi et al [16] published data from a prospective study of phobic anxiety and the risk of coronary artery disease, which included 34 thousand men who initially had no symptoms of cardiovascular disease. The identified relative risk of fatal CHD, taking into account the patient's age, was significantly higher in individuals with high levels of anxiety, even when adjusted for other potentially harmful variables. Interestingly, only the risk of sudden death increased. Kubansky [17] cites data from 10 prospective studies that confirmed the association of anxiety with coronary heart disease.

A conceptual model (Fig.) of the pathophysiology of the mechanism of action of acute and chronic stress in ischemic heart disease has been proposed [18]. Mental stress, acute or chronic, through the central nervous system causes a number of physiological responses, such as increases in circulating levels of catecholamines, heart rate and blood pressure, and platelet activation. The influence of these reactions on the activity of the cardiovascular system is determined by background factors, such as atherosclerosis, previous myocardial infarction, myocardial hypertrophy, and impaired contractile function of the left ventricle. Hypercatecholemia, tachycardia and increased blood pressure lead to increased myocardial oxygen demand and can cause the development of angina, myocardial infarction, arrhythmias, and sudden death.

The evidence supporting this conceptual model of the effects of stress in CAD is extensive. Many studies have identified hypothalamic-pituitary-adrenal hyperfunction in unmedicated patients with major depression. These studies showed increased cerebrospinal fluid concentrations of corticotropin-releasing factor (CRF) and inadequate suppression of cortisol secretion following dexamethasone administration. Post-mortem studies of the brains of depressed patients also provided direct evidence of an increase in the number of CRF neurons in the hypothalamus. In addition, many patients with major depression exhibit hyperfunction of the sympathoadrenal system. Hypersecretion of norepinephrine in patients with depression is evidenced by an increase in plasma concentrations of norepinephrine and its metabolites in the urine [19–25].

Possible mechanisms of depression and anxiety on the progression of coronary heart disease

According to the presented pathophysiological model, there is evidence to suggest that increased sympathetic tone is the main mechanism determining the poor prognosis of anxiety and depression in patients with CAD. Kawachi et al [30] published results of measuring heart rate variability in 581 people aged 47 to 56 years without coronary artery disease or diabetes mellitus. Heart rate variability was measured during deep breathing and defined as the permissible deviation of successive intervals between 2 successive R-waves on an electrocardiogram during normal sinus rhythm, reflecting the balance of sympathetic and parasympathetic influences on the heart. High heart rate variability is observed in healthy individuals, while patients with coronary artery disease or heart failure may show a significant decrease in heart rate variability.

Men with high levels of phobic anxiety had a higher resting heart rate (HR) (p = 0.25). After classifying patients by age, average heart rate, and body mass index, it was found that those with high levels of phobic anxiety had significantly lower heart rate variability (p = 0.03). These findings suggest that phobic anxiety is associated with impaired cardiac autonomic control and may be associated with an increased risk of sudden cardiac death.

However, whether the decrease in heart rate variability was the cause of concern or vice versa is still unclear. In addition, the researchers were not able to exclude the presence of subclinical CAD during the examination of patients. Heart rate variability was assessed using short-duration electrocardiogram (ECG) recordings, given that many previous studies have used 24-hour ECG recordings. However, the results obtained turned out to be very interesting.

The risk of subsequent cardinal events for patients with heart disease has been examined in numerous studies. It has been shown to be associated with decreased heart rate variability and/or increased sympathetic tone. A decrease in heart rate variability was observed in depressed patients when compared with non-depressed patients. Among patients with confirmed coronary artery disease, a decrease in heart rate variability when recording an ECG within 24 hours was more often detected in depressed patients than in patients without depression, when the latter had coronary disease of approximately the same severity. A decrease in heart rate variability indicates insufficient parasympathetic tone, which may be a risk factor for ventricular arrhythmias, increased platelet aggregation, and increased cardiovascular mortality.

R. Krinayaphong et al [31] studied changes in heart rate variability in daily life in patients with coronary artery disease but without clinical depression. The study confirmed that CAD patients with higher depression scores had lower heart rate variability. The same data regarding the effect of depression on heart rate variability in patients with coronary artery disease were obtained by Hathway SR McKineley [32]. Patients were grouped using the Minnesota Multidisciplinary Individual Depression Scale. It is important to note that clinically no patient was depressed. However, the study results showed that the standard deviation of the intervals (SDNN) was lower and the mean heart rate was higher in patients with higher depression scores (p=0.009 and p=0.003, respectively). Mean heart rate and SDNN were the only demographic or clinical factors that accounted for differences between groups. The authors attributed their findings to the already established association between depression and survival risk in patients with CAD. The clinical importance of this study is that it revealed the relationship between depressive tendencies and disturbances in heart rate variability in a population that is apparently not clinically depressed.

Myocardial ischemia as a response to mental stress

Several studies have shown that patients with coronary artery disease respond to acute mental stress testing by developing myocardial ischemia [33, 34]. In 50% of patients with coronary artery disease and positive exercise tests using radionuclide methods, signs of myocardial ischemia were detected in response to a psychological stress test. Jiang et al [33] followed 126 patients for 5 years. Patients whose ischemia was initially caused by acute mental stress had a significantly higher incidence of subsequent fatal and nonfatal cardiac events over the subsequent 5 years, independent of age, baseline left ventricular ejection fraction, and history of myocardial infarction. This study suggests that the link between mental stress and adverse cardiac events is myocardial ischemia. The PIMI (Psycho-physiologic Investigations in Myocardial Ischemia) study revealed the same patterns.

Acute mental stress reactions and chronic reactions, previously described in patients with depression and anxiety, had a number of common features. The PIMI also examined the relationship between heart rate variability and ischemic responses to neuropsychic stress [35]. Heart rate variability was measured before and during a psychological stress test in 147 patients with coronary artery disease. In 47 patients, radionuclide or ECG signs of ischemia were detected during neuropsychic stress. Analysis of heart rate variability indicates impaired autonomic reactions in patients in whom ischemia developed in response to neuropsychic stress. When conducting a stress test in patients with ischemia, as a response to neuropsychic stress, a more pronounced decrease in heart rate variability was revealed compared with the same indicators in patients without ischemia. These data suggest that ischemic responses to neuropsychic stress were combined with excessive sympathetic activation and/or insufficient vagal activation. Thus, the increased risk of cardiac events in patients with cardiac pathology may be partly due to mental stress and concomitant disturbances in the balance of the autonomic nervous system. In addition, acute mental stress and chronic depression and anxiety may have similar pathophysiological mechanisms in terms of predisposing patients to cardiovascular disasters and complement each other.

The influence of depression and anxiety on the functional state of platelets

The adverse effects of depression on cardiovascular disease may also be mediated through platelet mechanisms. Platelets have receptors for catecholamines and serotonin (5-HT). Increased levels of catecholamines, such as those found in depression, can cause platelet activation, including platelet aggregation and the development of acute coronary syndrome. When activated, platelets release granules that may contain chemotoxic and mitogenic factors that cause the movement of leukocytes and other factors such as platelet factor and serotonin. These factors stimulate and attract other platelets and cause vasoconstriction. Increased intracellular free calcium, 5-HT2 binding receptor density, and decreased serotonin transport sites predisposing to increased platelet aggregation have been described in patients with depression.

The influence exerted by the psychological state of patients on platelet aggregation in patients preparing for planned major surgical interventions is very clear. Most patients on the eve of surgery experience anxiety and fear; a number of patients exhibit depressive symptoms, which affects the state of the autonomic nervous system and platelet aggregation ability.

The addition of antidepressants to a previously used treatment regimen for coronary artery disease gave a positive therapeutic effect in 85.6% of cases: improved mood and decreased anxiety, decreased lability and asymmetry of blood pressure, decreased heart rate from 83±6.7 to 77±1.2 (p<0. 02) and the number of angina attacks at rest from 7±0.31 to 2±0.17 (p<0.01). In addition, patients who received an antidepressant in the preoperative period had a significantly lower level of platelet aggregation immediately before surgery (18±0.22 versus 21±0.67 mm/s, respectively p<0.01) compared with the indicators of patients who were not receiving antidepressants.

Impact of depression and anxiety on the management of patients with cardiovascular disease

There is no generally accepted concept for the management of patients with cardiovascular disease and comorbid depression and anxiety. First of all, it is necessary to improve the diagnosis of these diseases - most depression and anxiety disorders in somatic patients remain undiagnosed both in outpatient and inpatient settings. To evaluate the effect of antidepressant treatment on the survival of patients with cardiovascular diseases, the course of coronary artery disease, hypertension, work ability, recovery after myocardial infarction and cerebrovascular accidents, additional clinical studies are necessary.

A.A. Kirichenko, Doctor of Medical Sciences, Professor RMAPO, Moscow

Note!

Among patients with cardiovascular diseases, the frequency of concomitant depression is 22-33%
The relative risk of having major depression or depressive symptoms for progression to cardiovascular disease or cardiovascular mortality ranges from 1.5 to 4.5
The increased risk of cardiac events in patients with cardiac disease may be due in part to mental stress and concomitant disturbances in the balance of the autonomic nervous system.

What are the symptoms of pain in different diseases?

Often, pain in the heart area when inhaling is attributed to purely heart diseases, without even suspecting that the real reason lies in something completely different.
How the pain syndrome manifests itself depends on the causes and level of progression of the disease. For example, with heartburn, a burning sensation also occurs in the sternum area. They occur when gastric juice enters the esophagus. Heartburn is also characterized by the appearance of belching and an unpleasant sour taste. These symptoms appear after eating, when bending the body, or in a lying position. In this case, antacid medications are prescribed for relief. When heartburn occurs and pain radiates to the heart area, the cause does not always lie in the esophagus.

These may be symptoms of gastroesophageal reflux disease (GERD), which is also characterized by heartburn;
Spasm of the esophagus with disruption of muscle function, which leads to problems with swallowing and moving food in the stomach;
With achalasia, this pathology manifests itself in disruption of the valve between the stomach and esophagus, with food retention and the appearance of pain in the chest.

Depending on the nature of the pain in the heart area, inflammatory diseases can be diagnosed:

Gall bladder with the development of cholecystitis;
Pancreas and acute manifestations of pancreatitis;
Gallstone disease (GSD).

Painful symptoms in these diseases can radiate into the chest cavity and resemble heart pain.

Pulmonary diseases can also be accompanied by sharp and dull pain in the chest. These signs can occur with pneumonia, pleurisy , with characteristic inflammation of the lungs and tissues that line the chest cavity, respectively. These diseases are characterized by increased pain when inhaling, the appearance of a cough, and an increase in temperature to critical values. Also, diseases can accompany each other and after pneumonia complications arise, which manifest themselves in the form of pleurisy.

What to do to correct the situation

Seek advice from a psychotherapist, since the reason is not in the body, but in mental torment. He will help you understand the problem, find a solution, build a treatment plan, and also provide moral support on the path to recovery. In addition, if the symptoms are pronounced, constantly torment, or manifest themselves to an extreme degree, for example, panic attacks, then medications are prescribed to treat anxiety disorder. Most often these are sedatives, but antidepressants can also be prescribed. You should not be afraid of any of this, neither going to the doctor nor taking a course of medications. Anxiety disorder is the same disease as the flu. You won't be afraid to treat him. The sooner you seek help, the sooner you can return to normal life and get rid of heart pain and other unpleasant symptoms.

How to help with acute pain in the heart?

It is no coincidence that when pain appears in the heart area, they do not know what to do until the doctor arrives. Call the hotline number +7 (863) 226-18-17 , which is best entered into the phone’s memory in advance. Experienced private medical doctors help in emergency situations and transport the patient to the hospital. Emergency medical care is provided in clinics, hospitals and at home.

Before the doctor arrives, you should stop moving and take a lying position, and be sure to call a specialized ambulance. If your heart hurts, self-medication can end sadly and lead to death.

In case of high or low blood pressure, take the tablet as indicated. The patient is prescribed sedative drops , Corvalol, motherwort, valerian, and nitroglycerin. If the pain has passed, there is no need for nitroglycerin; it is also contraindicated for low blood pressure. You can put validol under your tongue. Treatment of cardiac pathologies is prescribed by a doctor according to indications.

What diseases cause pain in the heart?

Acute pain syndrome can also appear with pulmonary diseases such as bronchial asthma and pneumothorax. Asthma attacks cause pain throughout the chest cavity. An equally severe form and painful condition is characterized by pneumothorax , in which air penetrates from the outside into the chest cavity and the lungs can collapse with the appearance of pain.

Among the main causes of painful attacks in the sternum area is also pathology of the peripulmonary vessels. They intensify when inhaling with the formation of a cough with pulmonary embolism , pulmonary hypertension with increased pressure in the vascular system supplying blood to the lungs.

Painful vascular diseases include dissecting aortic aneurysm with characteristic damage to large vessels. This emergency condition can be life-threatening. In this case, the pain is initially felt in the heart area and gradually moves down the abdomen. The patient's blood pressure drops sharply, tachycardia occurs and he loses consciousness.

A classic example of the appearance of pain in the chest area is osteochondrosis , which occurs in the thoracic and cervical spine. The pain is reminiscent of angina attacks with radiation to the left shoulder blade and arm. The difference lies in the intensification when moving, raising arms, turning the head, bending the body.

Sharp stabbing pain is characteristic of intercostal neuralgia, Tietze syndrome . It occurs at the joints and spaces between the ribs and becomes more intense when inhaling. The patient cannot take a deep breath, shallow breathing is observed. In case of pathology, strong anti-inflammatory and painkillers are prescribed.

How else can you ease the attack?

Photo: Ivan Samkov/Pexels
There are a number of techniques to help cope with a panic attack.

First of all, you need to admit that you are having a panic attack, and not a stroke or heart attack, tell yourself that your life is not in danger and that this condition will gradually pass.

Some experts and experienced patients with this disorder recommend repeating a prepared phrase to yourself, for example, “Everything passes, and this will pass.”

In this case, you need to focus on breathing. A person can control this physiological process. Experts recommend inhaling air through your mouth, counting to four, holding your breath for a second, feeling how your chest is filled with air, and then exhaling just as slowly for four counts.

What follows is mutually exclusive advice, since different techniques help different people.

The first line of action is to close yourself off from external stimuli. It is recommended to close your eyes and relax your body muscles. It is advisable to master the muscle relaxation technique in advance so that it can be used effectively during an attack.

Another line of behavior is to use a technique called “grounding,” which can be translated into Russian as “grounding.” It is especially effective for those who, during a panic attack, experience a feeling of losing contact with reality.

To restore this contact and control over the situation, it is recommended to do something opposite to what was suggested above, namely:

listen to sounds;

take off your shoes and stamp your bare feet, feeling the structure of the surface underneath them;

touch the fabric of your clothes, the surface of the table, the objects you have in your bag with your hands, and realize the difference in sensations from smooth surfaces and soft or fluffy objects.

wrap yourself in a blanket, hug a plush toy and record the feeling of this action.

smell something odorous.

Experts and people who have experienced panic disorder recommend carrying around a helpful box with small objects that can trigger a variety of sensory sensations. These can be smooth and rough pebbles, small bottles of perfume or essential oils, pieces of fabrics of different textures.

How to understand that your heart hurts?

Pressing sharp pain in the heart occurs with angina pectoris or “angina pectoris,” which is the main precursor to the development of coronary heart disease (CHD). It radiates to the shoulder, left hand and little finger, and can radiate to the jaw. The intensity increases with nervous tension and physical activity. It occurs as a result of coronary vascular spasm and insufficient oxygen supply to the heart muscle due to atherosclerosis. The pain may go away on its own with rest and rest.

Among the most dangerous heart diseases associated with the cardiovascular system of the body is myocardial infarction . It occurs as a result of blockage (thrombosis) of a coronary artery by an atherosclerotic plaque and cessation of blood supply to an area of the heart muscle. In this case, necrosis occurs and part of the muscle dies.

Pain during myocardial infarction causes severe weakness, lack of air, radiates to the left arm, encircles the shoulder and spreads under the left shoulder blade, sometimes to the neck, jaw, and can form far from the heart area. Sometimes the temperature rises. The person breaks into a cold sweat, shortness of breath, and in some cases nausea.

Chest pain occurs in the case of cardiac pathologies of inflammatory etiology, these include endocarditis , myocarditis , pericarditis. They appear after illnesses caused by viral and bacterial infections.

Why does my heart hurt after excitement?

A psycho-emotional disorder of any origin (failure at work, loss of loved ones or watching an exciting film) is a significant burden on the body.
As a result of exposure to a stress factor, the brain sends a signal to the peripheral organs of the sympathoadrenal system - the adrenal glands. Their brain matter releases adrenaline and norepinephrine into the blood. Due to a hormonal surge, a number of changes occur:

vasoconstriction (narrowing of peripheral vessels), including coronary ones;
centralization of blood flow to vital organs (brain, heart, lungs);
stimulation of special receptors in the heart, blood vessels, bronchioles and adipose tissue.

Such pathophysiological changes lead to increased blood pressure, tachycardia (rapid heartbeat), rapid breathing, and pale skin.

Pain appears with irradiation, shortness of breath, tremor, dizziness, up to loss of consciousness.

The breakdown of adipose tissue leads to an increase in heat production. The body tries to maintain normal body temperature by releasing heat, which is why excessive sweating occurs.

The myocardial need for oxygen increases, but due to spasm of the coronary arteries (those that supply the heart) during diastole, not enough blood is supplied. Thus, demand exceeds capacity, which provokes ischemia. Against this background, chest pain occurs with symptoms of angina pectoris.

How is differential diagnosis carried out?

If chest pain occurs, you should immediately call an emergency doctor. Before the specialist arrives, if possible, relieve emotional and physical stress, calm down, lie down and understand the nature of the pain in order to properly notify the doctors.

The doctor's examination includes consultations with specialized specialists, instrumental studies, and an electrocardiogram. It shows how the heart works, detecting signs of a heart attack depending on the stage and location.

Medical care and consultations can be prescribed by various specialists, a neurologist, cardiac surgeon, infectious disease specialist, pulmonologist, surgeon, gastroenterologist, psychiatrist. In case of nervous experiences, you may need the help of a psychologist.

Instrumental studies

In addition to an electrocardiogram (ECG), in case of cardiac pathology, various instrumental diagnostic studies .

Ultrasound of the abdominal cavity;
FEGDS examination of the digestive organs;
Ultrasound of the heart, pulmonary vessels and aorta;
FVD, examination of external respiration functions;
Chest X-ray;
CT, computed tomography;
MRI, magnetic resonance imaging;
EchoCG, echocardiography and others.

What signs confirm heart pain?

Critical conditions are caused by cardiac pathologies, which can be determined using simple manipulations. It is necessary to understand whether the pain intensifies when inhaling, when raising your arms, bending your torso, or whether you can take a deep breath. An increase in pain may indicate the presence of intercostal neuralgia or osteochondrosis.

The pain may intensify with physical exertion and decrease at rest when angina pectoris , with insufficient blood supply to the heart muscle in an active state.

Cardiac pathologies are often accompanied by sharp pressing pain, difficulty breathing, stress, discomfort in the chest, cold sweat, irradiation to the left shoulder, arm and under the left shoulder blade.

An emergency call to a private medical ambulance allows you to help in emergency situations, do an ECG, a rapid blood test for the protein troponin to determine myocardial infarction, and transport the patient to the hospital.

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