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Stroke, arterial hypertension and left ventricular mechanics

Tadic, Marijana

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doi: 10.1097/HJH.0000000000001937
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The association between arterial hypertension, stroke and left ventricular (LV) structure, primarily LV hypertrophy (LVH) and LV geometry has been previously reported [1–3]. Investigators showed that LVH was associated with transient ischemic attack and stroke independently of the blood pressure level and other demographic and clinical characteristics [1–3]. Verdecchia et al.[4] reported that LVH regression was related with a significant reduction of risk of cerebrovascular event. The risk of cerebrovascular events was 2.8 times higher [95% confidence interval (CI) 1.18 – 6.69] in the subset with persistent LVH or new LVH development than in that with LVH regression or constantly normal LV mass. This effect was independent of age and 24 h SBP.

LV mechanical changes represent subtle impairment in LV function that is difficult to detect with conventional echocardiographic techniques. Investigations proved that LV longitudinal strain is superior to LV ejection fraction in the prediction of cardiovascular morbidity and mortality, as well as total mortality [5–7]. After these findings, the number of studies regarding LV longitudinal strain in different clinical settings significantly increased and nowadays the data regarding LV longitudinal strain are available in almost all cardiovascular diseases.

Hypertension has a significant impact on LV mechanics independently of LVH [8]. This is particularly valid for LV longitudinal and circumferential strain, whereas there are no consistent data regarding radial strain [8]. The finding of reduced LV longitudinal and circumferential strain in the hypertensive population is particularly important when one considers the high predictive value of LV mechanics for cardiovascular morbidity and mortality in the global and hypertensive population [9,10]. However, the relationship between arterial hypertension, stroke and LV mechanics has not been investigated so far.

In this issue of the Journal, Saeed et al.[11] reported significantly reduced LV global longitudinal strain (GLS) and global circumferential strain (GCS) in hypertensive patients with stroke. The prevalence of reduced GLS and GCS in the patients with stroke because of large artery atherosclerosis was 60 and 50%, respectively [11]. The corresponding prevalence among the patients with lacunar infarct was 76 and 52%, respectively. The researches revealed association between hypertension and GLS even after adjustment for LV mass, ejection fraction, male sex, obesity and diabetes, whereas the relationship between hypertension and reduced GCS disappeared.

There are several important points in this study that deserve further discussion and clarification. The current study did not investigate the relationship between GLS and stroke in hypertensive patients. The authors showed that hypertensive patients who suffered stroke had significantly lower values of GLS and GCS in comparison with their normotensive counterparts [11]. On the other hand, Russo et al.[12] demonstrated that lower GLS, but not LVEF, was associated with greater white matter hyperintensity volume in 439 participants free of stroke and cardiac disease. Su et al.[13] found a significant predictive value of LV GLS for cardiovascular events, particularly a new onset of cardiac failure and coronary artery disease, but not for stroke. Another interesting study in patients who were followed 5.5 years after acute myocardial infarction revealed that only GLS remained a significantly independent predictor of stroke and atrial fibrillation development after adjustment for important demographic and clinical predictors (age, sex, diabetes, hypertension, diastolic dysfunction, and LVEF) [14]. However, when outcomes were separated in two groups: atrial fibrillation and ischemic stroke, there was only borderline predictive significance of LV GLS (hazard ratio 1.15; 95% CI 0.99–1.32, P = 0.066] and statistically significant predictive value of LV GLS for atrial fibrillation development (hazard ratio1.18; 95% CI 1.01–1.37, P = 0.035) [14].

Saeed et al.[11] reported significantly reduced GLS and GCS in hypertensive patients who had stroke. This is in accordance with the majority of studies conducted in the hypertensive population [8,15]. It should be mentioned that hypertensive patients in the present study also had more prevalent other cardiovascular risk factors such as age, dyslipidemia, diabetes, obesity, metabolic syndrome and LVH. All these parameters have been previously recognized and well established as the risk factors that decrease LV GLS and GCS [16,17]. After adjustment for these factors, arterial hypertension still remained significantly associated with GLS, but not with GCS. This discrepancy supports the view that GLS is a more sensitive LV strain parameter in the hypertensive population than GCS. Considering the fact that endocardial and epicardial myocardial fibers are primarily responsible for GLS, whereas mid-myocardial fibers are more responsible for GCS, one could hypothesize that the first and subtle impairment in LV longitudinal function is the consequence of subendocardial damage in arterial hypertension. This could be the reason why GLS is a more reliable strain parameter than, for example, circumferential and radial strain.

The current study showed the trend of more deteriorated GLS than GCS in patients with almost all ischemic stroke subtypes [11]. However, statistical significance was reached only in the patients with lacunar infarct. If there is a relationship between different stroke subtypes and LV mechanics is difficult to say because the authors did not provide other relevant characteristics of the patients with various ischemic stroke subtypes. It would be interesting to further investigate this relationship in the future studies.

There are a couple of technical points that should be discussed in relation with the present study. First, the authors measured GLS only in apical four-axis and long-axis views, whereas the two-chamber view was not involved in the calculation because of the technical issues related with obtaining this basic echocardiographic view. This means that GLS was evaluated in 12 instead of 17 LV myocardial segments, which is an important limitation to the current study [11]. Similarly, LVEF was calculated with the biplane Simpson method by using four-axis and apical long-axis views. As the authors aimed to investigate LV longitudinal mechanics, it might have been better if they used only a four-chamber view when all three necessary apical views were not available, as some other authors used [6]. The authors’ intention to present as many as possible information in this article is clear and understandable; however, this kind of incomplete LV strain analysis should not be encouraged in the future. There are clear guidelines regarding speckle-tracking imaging and they should be followed in the scientific reports [18]. Second, the authors of the present study used peak systolic strain as the reference for GLS and GCS. This is also not recommended by the latest guidelines that proposed the usage of end-systolic strain [18]. In the current situation, there should not be significant difference between peak systolic strain and end-systolic strain simply because there were no patients with heart failure, ischemic heart disease or another cardiac disease that would significantly change the pattern of motion and mechanics during the cardiac cycle.

There are several mechanisms that could potentially explain the association between arterial hypertension and LV mechanics in stroke patients: LV hypertrophy; comorbidities; biohumoral mechanisms and hemodynamic changes related with arterial hypertension. LV mass is significantly increased in hypertensive patients in this study, which is a very important structural parameter related with reduced GLS and GCS [7,15]. Furthermore, comorbidities such as diabetes, obesity and metabolic syndrome significantly deteriorate LV mechanics. Previous studies showed not only their additive, but also synergistic negative effect on LV remodeling including LV strain. However, all these risk factors are based on biohumoral mechanisms that are common for hypertension-induced cardiac remodeling and often overlap with mechanisms typical for LV remodeling in patients with diabetes, obesity or metabolic syndrome. The most relevant putative mechanisms that could be responsible for hypertension-related LV mechanical changes are: the autonomic nervous system; activation of the renin–angiotensin–aldosterone system and its interaction with the sympathetic system; increased oxidative stress; and reduced concentration of natriuretic peptides (atrial and brain natriuretic peptides, calcitonin gene-related peptide). Hemodynamic changes typical for arterial hypertension such as increased preload at the beginning of hypertension and an increase in systemic vascular resistance afterwards or a combination of both could significantly contribute to deterioration of LV mechanics. At the histological level, these biohumoral and hemodynamic changes induce extracellular deposition of fibrin in the cardiac interstitium. This myocardial fibrosis is related with worsening of LV elasticity and subsequently with reduced LV mechanics.

LV GLS has an important predictive value for cardiovascular morbidity and mortality and it would be of great importance to conduct a longitudinal study, which would address the question of a possible predictive value of GLS in ischemic stroke occurrence. This study might provide valuable information and possible cut-off values of GLS (and perhaps GCS) for hypertensive patients who are at higher risk for stroke. The growing amount of evidence regarding the predictive value of GLS in the hypertensive population is indicating that LV GLS assessment should be introduced in routine echocardiographic evaluation of hypertensive patients. Obviously, hypertensive patients with lower GLS are at higher risk for stroke and they should be monitored more closely until we determine clear cut-off values for GLS that are associated with greater risk for cardiovascular and cerebrovascular events.


Conflicts of interest

There are no conflicts of interest.


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