Effects of Cardiovascular Disease Treatment on the Remodelling and Diastolic Characteristics of the Left Ventricle

Thomas Denney^*
*Correspondence: Thomas Denney, Department of Preventive Medicine, University of Valencia, Valencia, Spain, Email:

Keywords

Left ventricle • Cardiovascular disease • Diastolic dysfunction • Cardiac magnetic resonance imaging

Introduction

Cardiovascular breakdown is a significant clinical issue. In the right clinical setting, patients with preserved left ventricular (LV) ejection fraction (EF) are thought to have diastolic dysfunction and heart failure. The LV remodels in response to pressure, volume overload, or both are central to the pathogenesis of cardiac dysfunction. It is generally acknowledged that structural remodeling of the LV is closely linked to the mechanical properties of the LV. Increased LV wall stress as a result of elevated systolic blood pressure causes LV concentric remodeling and hypertrophy with increased chamber stiffness in hypertensive (HTN) patients, who are more likely to experience diastolic dysfunction. These are considered important characteristics of diastolic dysfunction. In contrast, eccentric LV remodeling may occur in other circumstances, such as after a myocardial infarction. These patients might show systolic brokenness. Concentric LV remodeling may eventually progress to dilated LV and systolic dysfunction in heart failure, according to some research. This conventional notion of HTN-associated LV remodeling, on the other hand, has been called into question [1].

In a recent study, we reported that participants with advanced LV diastolic hemodynamic abnormalities (increased LV end diastolic pressure, LVEDP, and the time constant of LV relaxation, τ,) and increased chamber stiffness surprisingly revealed relatively more eccentric LV geometry, versus more concentric LV geometry in those with better LV hemodynamic measurements and less chamber stiffness. This prompted us to test the hypothesis that such a contradiction to the expected relationship between LV concentricity and diastolic properties may be due to the effects of concomitant cardiovascular diseases, major cardiovascular disease risk factors (CVDRFs) and the corresponding medication therapy. This hypothesis relies on accumulated evidence that coronary artery disease (CAD) and all major CVDRFs including HTN, dyslipidemia (DL), and diabetes mellitus (DM) can be associated with impaired LV diastolic hemodynamic and mechanical properties. Therefore, using our well-characterized patient cohort, we undertook a detailed analysis of the relationship between concomitant CAD and major cardiovascular disease risk factors (CVDRFs) and corresponding medications with LV diastolic properties [2].

Literature Review

In subjects at risk for or in the early stages of heart failure with preserved LVEF, our study found a clear association between LV diastolic hemodynamic and mechanical derangements and "adequate" treatment of CAD & CVD RFs. Our analysis reveals that, in patients receiving adequate medical treatment for underlying CAD and CVD RFs, the severity of LV diastolic hemodynamic and mechanical derangements may not be directly related to the severity of underlying CAD and CVD RFs. As a result, it provides important insights for evaluating therapeutic options. According to our findings, patients who do not receive "adequate" medication therapy for CAD or CVD RFs are more likely to experience LV diastolic hemodynamic and mechanical abnormalities. Those with an increasing number of CVD RFs who are not taking "adequate" medications experience more severe derangements [3].

In the absence of hypertrophy, we discovered that improved diastolic hemodynamic and mechanical properties were associated with a more concentric LV. The commonplace worldview of LV renovating in cardiovascular breakdown with safeguarded LVEF is portrayed in view of raised systolic circulatory strain prompting concentric LV rebuilding/hypertrophy to standardize systolic wall pressure, which may ultimately become dysregulated with ensuing dilatation of the LV in the last option phases of cardiovascular breakdown. Participants at risk for heart failure with preserved LVEF were included in our study, but we did not a priori select patients with concentric LV hypertrophy. It may be an adaptive mechanism to preserve a satisfactory LV diastolic function in a relatively normal size heart before the heart becomes hypertrophic with compromised and stiff myocardium. In our study cohort, a relatively more concentric LV without hypertrophy was associated with a decreased LV diastolic wall stress. The LV mass increase in DM patients without HTN or ischemic heart disease may be partially explained by this speculative reasoning. In a subgroup of DM and HTN participants who exhibited increased LV mass and LV mass to volume ratio, this would be in line with somewhat decreased LV diastolic wall stress [4].

Discussion

The LV mass qualities in the ongoing review were middle between sound controls and those with uncontrolled HTN as detailed by us beforehand. Prescriptions including nitrate, statins, angiotensin changing over chemical inhibitors, angiotensin II sort 1 receptor blockers, calcium channel blockers, diuretics, and beta blockers, may likewise add to LV rebuilding and forestall the widening of LV in cardiovascular breakdown with protected LVEF. A somewhat more eccentric LV was also observed in participants who were not receiving "adequate" therapy and had obvious diastolic dysfunction. Despite its simplicity, our model identified a set of consistent and significant associations between changes in LV diastolic hemodynamic and mechanical properties, LV concentricity, LV preload, and the number of CAD & CVD RFs without "adequate" medication. This suggests that the effects on LV diastolic function could be mitigated if these abnormalities are treated [5].

Symptomatic CAD that was not treated with nitrates was associated with a significant portion of subjects who had impaired LV diastolic hemodynamic and mechanical properties, which directly increase coronary blood flow by vasodilating cardiac vessels. According to our findings, this may play a significant role in maintaining the mechanical properties of the LV in patients with symptomatic CAD. Curiously, calcium channel blockers, what share with nitrates a typical vasodilator impact on coronary stream, likewise uncover by and large helpful impacts in computer aided design companion. Echocardiographic studies have exhibited that whimsical hypertrophy is normal in numerous hypertensive populaces, but it was not known whether such patients had predecessor concentric hypertrophy [6].

Subsequently, a significant commitment of leftover C to remaining gamble could be anticipated in these members. Second, the majority of previous studies that demonstrated a causal link between remnant-C and cardiovascular disease (CVD) were carried out on population samples from north European and American populations. In Mediterranean regions, where a culturally driven dietary pattern was thought to explain part of the lower incidence of cardiovascular events compared to northern Europe or the United States, there was little evidence for the role of remnant-C in CVD risk. Additionally, this study's analytical models addressed potential confounding factors in the relationship between remnant-C and CVD risk. Information were adapted to potential modulators of TRL science, like weight, diabetes, sex, and way of life factors. Furthermore, the findings were unaffected by any ongoing lipid-lowering treatment. A portion of the participants' residual CVD risk was also explained by elevated remnant-C, according to studies of statin-treated cohorts. Patients with high remnant-C levels were more likely to develop coronary artery disease, even when treated with statins [7].

Echocardiographic studies have exhibited that whimsical hypertrophy is normal in numerous hypertensive populaces, but it was not known whether such patients had predecessor concentric hypertrophy. In an enormous report (The Dallas heart study, n=1282), the examiners recommended that the change of concentric LV hypertrophy to widened cardiomyopathy might be more uncommon. Furthermore, a new work dissecting echocardiographic information from the first Framingham Heart Study members likewise uncover a high pervasiveness of unusual hypertrophy in a moderately aged populace (around 50 years of age). Surprisingly, this cohort's 4-year follow-up data revealed a natural history of variable LV geometry changes [8].

In that study, older age, male sex, elevated systolic blood pressure, and obesity were the primary risk factors for abnormal LV geometry. Only the completeness of medication therapy was the primary factor affecting the LV geometry in our study, which only provides a snapshot of a medically treated symptomatic outpatient cohort at a single time point. Previous research primarily focused on the effects of medications on LV mass reduction in hypertensive heart disease patients with LV hypertrophy or diabetic patients to reduce LV concentricity, both of which are associated with poor cardiovascular outcomes. However, the relationship between LV concentricity and LV filling hemodynamic abnormalities in patients with normal LV mass and size is unknown. As LV mass was not elevated, our findings suggest that a significant subset of subjects with more eccentric hearts may develop LV diastolic dysfunction. These individuals may also progress directly to heart failure with LV dilatation or hypertrophy and may not have demonstrated antecedent concentric hypertrophy. This requires more investigation [9,10].

Conclusion

All concomitant CAD & CVD RFs with risk factors for/at early stages of heart failure with preserved LVEF appear to have a distinct association with LV concentricity, LV diastolic hemodynamic and mechanical derangements, and adequacy of therapy. In conclusion, our findings suggest that this association exists. This idea needs to be validated in a prospective study because if it is found to be true, it could have important implications for selecting the best individualized therapy and planning clinical trials.

Acknowledgement

None

Conflict of Interest

None

References

1. Brunzell, John D., Michael Davidson, Curt D. Furberg and Ronald B. Goldberg, et al. "Lipoprotein management in patients with cardiometabolic risk: Consensus statement from the American Diabetes Association and the American College of Cardiology Foundation." Diabetes Care 31 (2008): 811-822.

Google Scholar, Crossref, Indexed at

2. Chapman, M. John, Henry N. Ginsberg, Pierre Amarenco and Felicita Andreotti, et al. "Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: Evidence and guidance for management." Eur Heart J 32 (2011): 1345-1361.

Google Scholar, Crossref, Indexed at

3. Varbo, Anette and Børge G. Nordestgaard. "Nonfasting triglycerides, low-density lipoprotein cholesterol, and heart failure risk: two cohort studies of 113 554 individuals." Arterioscler Thromb Vasc Biol 38 (2018): 464-472.

Google Scholar, Crossref, Indexed at

4. Musunuru, Kiran. "Atherogenic dyslipidemia: Cardiovascular risk and dietary intervention." Lipids 45 (2010): 907-914.

Google Scholar, Crossref, Indexed at

5. Goldberg, Ira J., Robert H. Eckel and Ruth McPherson. "Triglycerides and heart disease: Still a hypothesis?" Arterioscler Thromb Vasc Biol 31 (2011): 1716-1725.

Google Scholar, Crossref, Indexed at

6. Schwartz, Gregory G., Markus Abt, Weihang Bao and David DeMicco, et al. "Fasting triglycerides predict recurrent ischemic events in patients with acute coronary syndrome treated with statins." J Am Coll Cardiol 65 (2015): 2267-2275.

Google Scholar, Crossref, Indexed at

7. Taskinen, Marja-Riitta and Jan Borén. "New insights into the pathophysiology of dyslipidemia in type 2 diabetes." Atherosclerosis 239 (2015): 483-495.

Google Scholar, Crossref, Indexed at

8. Nordestgaard, Børge G. and Anette Varbo. "Triglycerides and cardiovascular disease." Lancet 384 (2014): 626-635.

Google Scholar, Crossref, Indexed at

9. Nordestgaard, Børge G., Marianne Benn, Peter Schnohr and Anne Tybjærg-Hansen. "Nonfasting triglycerides and risk of myocardial infarction, ischemic heart disease, and death in men and women." JAMA 298 (2007): 299-308.

Google Scholar, Crossref, Indexed at

10. Estruch, Ramon, Miguel Angel Martínez-González, Dolores Corella and Jordi Salas-Salvadó, et al. "Effects of a Mediterranean-style diet on cardiovascular risk factors: A randomized trial." Ann Internal Med 145 (2006): 1-11.

Google Scholar, Crossref, Indexed at