1. Introduction
Chest pain is one of the common reasons for patients to seek urgent medical attention. By systematically evaluating the characteristics of the pain, the clinician can often determine the probable cause of the pain from the patient’s history. Angina pectoris is a pain syndrome with identifiable characteristics, and can determine if a patient’s pain is typical of angina pectoris by carefully analyzing all aspects of the patient’s history. Patients with angina-like pain are more likely to have obstructive coronary disease than those with atypical pain syndromes, as confirmed by coronary arteriography investigations.[
1] Patients with angina often describe the discomfort as dull, heavy, or crushing, and they may feel a pressing sensation instead of pain. Sharp, stabbing or burning pain is less common with angina. Anginal pain is usually felt as substernal or anterior chest discomfort, and it often spreads to the left arm in patients with coronary artery disease. About half of patients who experience recurring chest discomfort without coronary artery disease may have reflux esophagitis or esophageal contraction anomalies.[
2]
Myocardial infarction is one of the common causes of acute chest pain that requires rapid medical attention. The quality and location of myocardial infarction pain are comparable to angina pectoris, but it is often more severe and longer-lasting. Nitroglycerin may not relieve pain when the patient experiences it at rest. In acute myocardial infarction, identifying the occluded vessel is crucial for several reasons viz. determining the appropriate artery for dilation and stenting especially in multivessel disease, quantifying the lesion severity and its significance, comparing with echocardiographic findings of hypokinesia or akinesia, and distinguishing recent from old occlusions. The diagnosis, management, and prognosis of myocardial infarction rely heavily on ST-segment changes observed in the 12-lead electrocardiogram.[
3] However, only 70% of patients show new Q waves or ST segment elevations on their initial Electrocardiogram (ECG). Therefore, the absence of these signs does not rule out infarction.[
2] Chest discomfort is one of the most common sign of an acute Myocardial Infarction (MI), and pain radiation and site are also important, although few studies have investigated these factors. This study explored the relationship between the location of angina and the affected coronary vessel. Establishing a successful correlation could improve diagnostic accuracy, facilitate early intervention, help optimize treatment planning and resource utilization, and provide a basis for developing decision-support tools or algorithms to help healthcare providers rapidly assess and manage patients with chest pain.
Materials and Method:
This observational study analyzed consecutive patients of Acute Coronary Syndrome (ACS) between the age group of 18 years to 80 years who were admitted to a tertiary care Medical Institute between January 2017 and December 2019. The ethical clearance was obtained from the Institutional Ethical Committee. The cases were grouped in age intervals by decades.
Exclusion criteria: Patients with a known past history of coronary artery disease with or without previous Myocardial Infarction, non-obstructive heart disease or other established cardiac illnesses and those who had undergone angioplasty or coronary artery bypass grafting (CABG) surgery previously were excluded to avoid biases.
The following variables were evaluated : a) Age and gender demographic variables; b) the topography of angina and site of vessel involvement and c) The type of ACS.
Anginal Pain topography was recorded in a pictorial format for the sites where the patient reported pain, as illustrated in Illustration 1.
Each of the 411 patients was asked to mark all the areas he/she experienced chest pain prior to undergoing coronary angiography to avoid observer or reporting bias. E.g. If subject experienced pain in retrosternal, jaw and back area it was marked as area 1,2,8 (See Illustration 1). All the datasets were captured in tabular form in cumulative frequency and the final yield is plotted in Tables 2 and 3.
Illustration 1. Pictorial format for all the sites where patient experienced pain. Sites marked in green correspond to the example provided above. 1- Retrosternal, 2- Jaw Neck ,3- Left Shoulder ,4- Right Shoulder ,5- Right Arm ,6- Left Arm 7- Epigastrium 8- Back. Red color depicts the potential sites while green color highlights the site of pain experienced by the patient.
Discussion:
Ischemic episodes in angina pectoris trigger chemosensitive and mechano- receptors in the heart.[
4] This often occurs due to fissures or erosions of atherosclerotic plaques, which are common in ischemic syndromes like myocardial infarction and unstable angina. These events lead to the release of various chemical mediators into the coronary artery lumen, including serotonin, histamine, thromboxane A2, bradykinin, reactive oxygen species, lactic acid, and adenosine. These mediators, generated through the cyclooxygenase pathway, include prostaglandins (PGE2 and PGI2).[
4]
These chemical mediators interact with specific receptors, predominantly on chemically sensitive terminals, which depolarize cardiac visceral spinal afferent fibers. The cell bodies of these fibers, originating from the heart and coronary arteries, are located in the dorsal root ganglia (DRG) of the T2-T6 spinal segments, potentially extending to the C8-T9 segments.[
5] Chemo-sensitive nociceptors and mechanoreceptors innervate the epicardium, their excitation triggering pain, activating protective reflexes, and modulating cardiac function.
Sensitization of nociceptors occurs following injury or inflammation, with the release of prostaglandins, leukotrienes, substance P, and other mediators aggravating the condition. Unstable coronary atherosclerotic plaques can rupture or erode, activating platelets and releasing sensitizing chemicals that inflame the coronary arteries’ adventitia.[
6,
7,
8,
9] This activation of silent nociceptors and sensitization of chemosensitive receptors intensify the pain experience, particularly in patients infused with adenosine.[
10]
Prostaglandins, lipid autacoids derived from arachidonic acid via the cyclooxygenase pathway, are found in elevated concentrations in the plasma of patients with unstable angina pectoris or acute myocardial infarction.[
11]
Despite the pathophysiology of chest pain being understood, the localization of chest pain and pain pathways from the site of ischemia is not appropriately studied. The reasons are threefold. There is a paucity of sensory endings to the heart, a limited number of secondary sensory fibers in the spinothalamic tracts, and an absence of cortical area for localization of visceral pain in the post-central gyrus. The dermatomal distribution of pain fibers around the involved coronary and the corresponding segments of the spinal cord can, however, explain the relation and fill the existing lacunae.[
12]
Our research has identified a strong link between the location of retrosternal pain and the blocked artery. The chest pain’s location is crucial for diagnosing ACS/AMI. Pain in the center of the chest is more likely to be ischemic compared to pain located peripherally, with retrosternal chest pain being the most prevalent. In our study, 353 patients (59.9%) experienced retrosternal chest pain. Lichstein et al.’s study, which examined the relationship between chest pain location and coronary artery occlusion, found that the majority of patients (68.11%) had left precordial pain, with a significantly high probability (0.69) of Left Anterior Descending (LAD) artery occlusion.[
13]
De Silva et al. noticed that precordial and retrosternal sites are the most common sites for chest pain in Coronary Artery Disease (CAD).[
14] Bosner et al. analyzed 1212 patients (534 men and 678 women) for the etiology of their chest pain; of those, 180 patients (92 men and 88 women) were diagnosed with Coronary Heart Disease. The pain was present on the left side of the chest in 56 (63.6%) females and 63 (68.5%) males.[
15] Lichstein et al. and Bosner et al. noticed that chest pain was localized on the right side of the chest in 11.5% and 17.2 % of patients respectively. Another study by Swap et al. showed positive likelihood ratio of 4.7 (1.9-12.0) of chest pain radiating to right arm or shoulder with the diagnosis of Acute Myocardial Infarction.[
16] However, in our settings, none of the patients presented with right-sided chest pain. Leong et al also found that patients with chest pain were associated with LAD coronary artery occlusion in their study group. [
17]
According to a study by From et al., 1,077 patients (72%) presented with STEMI and 423 (28%) presented with NSTEMI. In that study, only 127 patients (12%) with STEMI had a culprit lesion in the Left Circumflex (LCX) artery compared to 166 patients (39%) presenting with NSTEMI.[
18] In our study, LCX was the culprit vessel in 33 (10.4%) patients with STEMI and 20 (21.7%) patients with NSTEMI. LCX was the second most commonly involved vessel after LAD in NSTEMI patients which is similar to the findings in the study by From et al. In contrast, in STEMI patients, LCX occlusion came third after LAD and Right Coronary Artery (RCA) occlusion in decreasing order of the involvement. Affected LCX occlusion was significantly associated with sites of chest pain at ’Jaw + Neck’ and ’Backache + Shoulder’ with positive correlations of 0.647 and 0.585, respectively.
In our study, RCA was the third most commonly affected vessel in patients with NSTEMI and second to LAD in patients with STEMI. RCA occlusion was significantly associated with sites ’Retrosternal + Jaw + Neck’ and ’Retrosternal + Backache’ with a positive correlation of 0.713 and 0.719, respectively. In the study by Karwoski et al., RCA and LCX were the most common infarct-related arteries in patients with STEMI and NSTEMI, respectively.[
19] This is in contrast to our study. However, what can be found from their study is that STEMI Patients with total occlusion of LAD had higher mortality on follow-up at 36 months of follow-up compared to NSTEMI patients, which showed no differences in mortality between total occlusion and near total occlusion.
STEMI and NSTEMI present with similar complaints of chest pain. The management of these two entities differs, which makes it essential to differentiate them.[
3,
20] The initial management of left and right coronary circulation involvement is different, making it essential to identify the occlusion site correctly.[
21] In cases of multi-vessel disease, particularly in NSTEMI where the identification of the culprit vessel based solely on ECG can be unclear, the use of angina topography can be instrumental in pinpointing the lesion that requires immediate attention. This method, in conjunction with ECG and imaging techniques like echocardiography, can enhance the accuracy of the diagnosis and the prioritization of treatment interventions which will help deliver timely intervention and improve outcomes.[
22] Also, in the acute setting of ACS, utilizing angina topography alongside ECG and imaging can assist clinicians in selecting the appropriate guiding catheter with the intent to revascularize, rather than a diagnostic catheter upfront to save time. These strategic choices can significantly reduce door-to-balloon time, thereby improving the overall efficiency and effectiveness of the emergency cardiac care provided.[
23]
The results of this study could contribute to improving patient communication and education in healthcare settings. Clinicians can utilize the understanding of chest pain patterns and their relationship with coronary artery pathology to inform patients about their condition prior to utilizing invasive diagnostic techniques. For instance, based on the study’s findings, a patient who presents with retrosternal pain spreading to the jaw and neck may be indicative of a right coronary artery (RCA) infarction, which is linked with the onset of symptoms such as nausea and vomiting,[
24] and an elevated risk of developing complete heart block.[
25] Also, nitrates should be avoided in patients with suspected right ventricular MI with RCA involvement.[
26,
27] Such likely adverse events can be explained to the patient beforehand leading to increased clarity about their own condition and improving doctor patient relationship.
Figure 1.
Flowchart demonstrating application of this study.
Figure 1.
Flowchart demonstrating application of this study.
The Limitations of our study include the small sample size of 411 patients admitted to a single tertiary care center. Even though the association between the site of pain and the vessel involved was statistically significant, a larger sample size with collaboration from multiple centers can strengthen the findings and help provide readily available information in the form of charts in rural areas. Secondly, chest pain and its location are subjective, and it is difficult to correlate it objectively. This may create a bias. Future developments of tools or models to identify the pain location may help resolve this bias. Future studies and models to identify the dermatomal distribution of pain can help solve this subjective bias. Another limitation is the lack of clarity in interpretation of the data for the multivessel involvement and chest pain location. Multiple coronary vessels are often involved, which requires more extensive multicentric studies to justify the findings. To aptly justify the value of studies, we recommend participation from smaller centers to be involved in the study. Based on our limitations and findings, we recommend more extensive studies in the future with multicentric involvement, training of medical professionals to interpret symptoms and findings, availability of rapid kits at an affordable rate, models to predict the location of pain and vessel involved from collaboration at larger centers, and finding the dermatomal association between them.