SAP has become a significant medical problem within the community, although it receives less attention in general cardiology practice. The principal objectives in the management of SAP to both acute and chronic forms mainly include the prevention of great cardiac events and the improvement of health status (Beltrame, 2017
). Clinically, SAP patients have three key components: angina symptoms, various functional limitations, and poor health quality, and each of these components is directly related to MI or mortality, therefore the importance of evaluating these patients is obvious, especially considering the chronic nature of the disease (Beltrame, 2017
). In this regard, LVEF is the most commonly used echocardiographic parameter to assess cardiac function and status in cardiology, where it is essential to guide therapy and for prognostication (Yeboah et al.
). Still, echocardiography as a “gold standard” image modality is recommended for assessment of patients in SAP, but it has limitations including high inter- and intra-observer variability. In our study, both control and CAD group patients had LVEF ⩾60%, so according to the value judgment, whey were “clinically normal”. But in the study, over 80% of both group patients had some symptoms of myocardial ischemia. Looking from the clinical perspective, STE has already been used for assessing ischemia-related myocardial and systemic diseases, where it can predict probable subclinical cardiac disorder earlier in the course of the disease, when conventional 2D echocardiography appears to be normal (Aggeli et al.
). STE should provide more information on the rate of segmental and global myocardial deformation such as factors for early cardiac pathology detection, herewith this method has been systematically validated to sonomicrometry, tagged MRI and colour-coded tissue Doppler echocardiography (Vanoverschelde and Goffinet, 2007
; Amundsen et al.
GLS is useful for detecting both significant and limitary (⩽70%) coronary artery stenosis during stress tests even at rest (Rosamond et al.
; Biering-Sørensen et al.
). It provides an insight into the longitudinal, circumferential, and radial mechanics of the heart and valuable insights to myocardial deformation by quantifying strain and torsion with the inherent advantage of being angle-independent (Nesbitt et al.
; Huang and Orde, 2013
). According to Biering-Sorensen, GLS can identify which concrete coronary artery suffers from significant stenosis. GLS was significantly lower in patients with CAD compared to patients without CAD and remained an independent predictor of CAD after multivariable adjustment for baseline data, exercise ECG and conventional echocardiographic parameters (Biering-Sørensen et al.
). Interestingly, longitudinally orientated myocardial fibres are located on subendocardial layers, the area most susceptible to ischemia, that is why measurements of longitudinal motion and deformation may be the most sensitive markers of CAD using tissue Doppler imaging (TDI) or 2-dimensional strain echocardiography (2DSE) (Biering-Sørensen et al.
; Hoffmann et al.
). We found an improvement of parameters in GLS longitudinal strain (LAD and LCX) on CAD and GLS circumferential strain in control groups, respectively. The vast majority of studies show the benefits of STE in identifying early CAD features when the results of other studies are uncertain. In opposite, the main findings of our study demonstrate that STE at rest is not suitable for the evaluation of the hemodynamical significance of coronary artery stenosis which is smaller than 70%. During an observation period of 2 years, we detected an improvement of measured parameters of STE. It means that the clinical condition of our patients over the two years has improved in both control and CAD groups. We, therefore, speculate that microvascular angina (MVA) may be responsible for this. Many patients at the initial stage of SAP and evidence of myocardial ischemia do not have a detectable or significant range of coronary atherosclerosis at CAA. Primary stable MVA defines patients with SAP, positive stress test results, and angiographically normal coronary arteries (Montalescot et al.
). The origin of MVA leading to functional abnormalities of coronary resistive vessels is not yet determined because of the heterogeneous entity and multiple pathophysiological mechanisms. Depending on the pathogenetic mechanism, there are 4 types of clinical classification of coronary microvascular dysfunction (CMD) according to the original classification proposed by Camici and Crea (Camici and Crea, 2007
). Standardized diagnostic clinical criteria for evaluation of MVA are as follows: (1) symptoms of myocardial ischemia, (2) absence of obstructive CAD (<50% diameter reduction or FFR > 0.80), (3) objective evidence of myocardial ischemia and (4) evidence of impaired coronary microvascular function (Ong et al.
). Definitively, MVA is diagnosed if all four criteria are present. Suspected MVA (sMVA) is diagnosed if symptoms of ischemia are present (criteria-1) with no obstructive coronary artery disease (criteria-2) but only objective evidence of myocardial ischemia (criteria-3), or evidence of impaired coronary microvascular function (criteria-4) alone, respectively (Ong et al.
). In our study, all patients both in control and CAD groups had evidence of three criteria mentioned above. These findings could be partially explained by the suitable treating of sMVA. Angina caused by coronary microvascular dysfunction in a sizeable proportion of patients undergoing CAA for anginal symptoms is found to show normal coronary arteries or nonobstructive CAD (stenosis <70%). For many years, there was uncertainty regarding the real significance of anginal symptoms that are accompanied by electrocardiographic evidence of ischemia during stress. In 1988, Cannon and Epstein demonstrated that compared with asymptomatic controls, in patients with chest pain and on CAA normal coronary arteries the coronary microcirculation has a heightened sensitivity to vasoconstrictor stimuli and a limited microvascular vasodilator capacity during atrial pacing which is allusive with the presence of MVA. The main goal of treatment of MVA is global risk factor control and anti-anginal treatment possibly targeting both large epicardial coronary arteries and coronary microcirculation (Crea et al.
). Common treatment mainly includes ACE inhibitors, statins, B-blockers, Ca channel blockers, antithrombotic, and nitrates. All our groups’ patients had this treatment during the two years (Table 1
). In our opinion, this fact has led to an improvement of STE. Even though drugs can help alleviate symptoms, many patients still have refractory symptoms, and treatment of these patients remains challenging. Atherosclerosis of small coronary arteries and its’ caused MVD affects myocardial longitudinal strain. Our study has shown that measurements of longitudinal strain could be useful when evaluating dynamic of myocardial function in SAP with nonobstructive coronary arteries.
Patients with MVD had significantly impaired diastolic function compared with healthy individuals. Moreover, improvement in GLS (−18.88 ± 0.48% vs. −20.52 ± 0.57%; $p<0.006$; LAD) and (−17.9 ± 0.87% vs. −19.78 ± 0.86%; $p<0.049$; LCX) should be interpreted as a possible result of MVD successful therapeutical correction both in “healthy” control and CAD patients.