Abstract
In recent time, the heart failure disease (HF) is advancing to be a global epidemic that results in substantive mortality in the population. In addition, heart failure contributes immensely to an increased cost of healthcare expenditures and also it’s a burden to the families affected. In the last three decades, there has been significant milestones in the treatment of heart failure with aldosterone antagonists, resynchronization therapy, angiotensin-converting enzyme (ACE) and beta receptor blockers. Nevertheless, the epidemic is still attributed to weak prognosis. Nevertheless, it has been approximated that half of the people diagnosed with heart failure demise within their first 5 years of treatment. Therefore, the major challenge is the search for better treatment of HF. In-depth comprehension, of the humoral perturbation and molecular compositions, will ultimately lead to fewer heart failure treatment.in this paper, pathophysiology, pharmacological and non-pharmacological intervention strategies of HF are discussed in detail.
Heart failure is a fatal and long-term illness that progressively gets worse over some time. The heart failure advances when the heart fails to pump blood throughout the body with the rate proportionate to the essentials of the metabolizing tissues (Azad& Lemay 2014). In this case, the heart is only able to pump blood under the conditioning of an elevated diastolic filling pressure. In addition, heart failure is highly characterized by abnormalities such as cardiac, renal, skeletal muscle, nervous system and neurohormonal changes (Eckel, et al 2014). The primary basis of the failure is the abnormality of the left ventricular function. This led to falling to a malfunctioning of the cardiac system. The fall of the cardiac system often leads to stimulation of neurohormonal mechanisms that reinforce the mechanical environment of the cardiac system.in addition, the activation of the sympathetic system tries to assist the cardiac system from falling out in case of impairment of left ventricle function. In an attempt to prevent the fallout, the heart rate is increased, increased catecholamine, increased myocardial contractility (Tham, et al 2015) Also, activation of renin system (RAAS) also causes vasoconstriction and increase volumes of blood, In this case, salt and water are preserved. Nevertheless, the cardiac dilatation and alterations progressively occur in the cardiac system (Yancy, et al 2013)
Medical attention for heart failure calls for different types of interventions to successfully cure it. The intervention strategy primarily depend s on the severity of the illness. There are two kinds of therapies; pharmacologic and non-pharmacologic therapies (Florea &Cohn 2014.) Pharmacologic therapy includes the use of vasodilators, diuretics, inotropic agents, anticoagulants, beta blockers, and digoxin. On the other hand, non-pharmacologic therapies include appropriate physical activities, dietary sodium and fluid restriction and attention to weight gain .In addition, more advanced therapies of cardiac failure include pacemakers, cardiac resynchronization therapy (CRT), Implantable Cardioverter-defibrillators (ICDs), revascularization procedures such as percutaneous coronary intervention (PCI), Coronary Artery Bypass Grafting (CABG), ventricular restoration and valve replacement and repair (Doehner, Frenneaux& Anker 2014.) There are three main forces reinforces the process of chronic heart failure, these are intrinsic myocardial damage, abnormality of the left ventricle, and other extrinsic factors that affect the heart itself.
Initiation of Heart Failure
Most of the cases of heart failure are caused by ischemia and infarction resulting in coronary artery disease (Basuray, et al 2014.) Other possible causes of heart failure include autoimmune infections, injuries metabolic and toxic insults. These toxic and metabolic substances include hyperthyroidism, alcohol toxicity, and doxorubicin toxicity. Extrinsic heart failure causes include anemia and arteriovenous fistula .In addiction, extrinsic causes are essential to identify since they are often fully reversible if identified early. An abnormal load in the cardiac system are caused by chronic blood pressures (Lymperopoulos, Rengo& Koch 2013)
Progression of Heart Failure
The mechanism behind the progression of the heart failure is basically ventricular remodeling after the initial insult. It’s crucial to note that, the initial; insult sets on a pace of destructive cycle where normal myocardium is severely altered resulting to hypertrophy and fibrosis (Desai , et al 2015).In addition, these cellular alterations led to changes in the in the structural features of the ventricle via the process known as remodeling. Therefore, remodeling often leads to the less efficient functioning of the heart thereby resulting in acute development of heart failure. Systemic is the main source of the pressure in the heart (Cruz, et al 2014). This results in reactivation of growth inhibitors that are present in the embryonic heart but absent in an adult heart. These factors act as a catalyst since they reinforce manufacturing of protein and myocyte growth. As a result, the myocytes increase in size while their numbers remain constant. This results in hypertrophy of the ventricle. With time diastolic dysfunction and systolic dysfunction causes the ventricle to be large, dilated and poor contraction (Segura, Frazier & Buja 2014).Another factor that sets in remodeling into motion is the myocardial infarction. In this case, the irreversibly injured myocardium ceases to function resulting in an overload of the remaining myocardium. This overload led to ventricular remodeling and subsequent dilation of the heart, thereby resulting in full ventricular dysfunction.
Pharmacological Intervention
ACE inhibitors
Comprehension of the fundamental mechanisms that cause the progressive heart failure, has resulted in the development of various pharmacological interventions. Among these interventions are inhibitors of the mediators that are involved in vasoconstriction and inefficient processes in the heart failure. The ACE inhibitors and angiotensin –II receptor antagonists inhibit renin-angiotensin-aldosterone system which has contributed positively to the treatment of chronic heart failure. In the last 2 decades, it has resulted in the improvement of the treatment of both the symptoms and the disease (Clark, Fonarow, & Horwich 2014. Recent studies have shown that patients with asymptomatic systolic dysfunction greatly benefit from this ACE-1 therapy. In addition, these agents not only helps in improvement of the hemodynamics but also exhibit the ability to slow the progression rate of myocardial damage at the tissue level, also it favorably alters remodeling.( Senni, et al 2014)
Beta-blockers
In pharmacologic interventions, inhibition of neuroendocrine is possible whereβ-blockers are used to treat heart failure. The Nonselective beta-blocker is used to ease the symptoms and the systolic components of the heart to prolong life. Beta- blockers work by decelerating the heart rate which permits the left ventricle to fill completely and propel blood more efficiently (Mann& Felker 2014). Further, it also works well in opening or widening of the blood vessels to allow more blood to flow. Examples of beta blockers include metoprolol, bisoprolol, and carvedilol
The Mechanical unloading
The utilization of implantable left ventricular assist device (LVAD) has illuminated more light in the study and treatment of the HF. In the research done by the Texas heart institute they found out that LVAD was possible to support the life of the patients for 503 days (Ponikowski, et al 2014). Additionally, the patient succumbed to neurologic complexities, recent studies have shown that LVAD support can assist the patients for more than 30 days. It improves it improves hemodynamics and histologic markers of the cardiac system such as endocytosis. However, other studies suggest that LVAD support improves the phenotype of fibrosis and pathologic hypertrophy. Therefore, alteration of the hemodynamics slows the progression of a heart failure and it reverses maladaptive processes (Roger 2013). The outcome of these studies might help to understand and establish the terminal threshold that terminates the functioning of the left ventricular system.
Genetics of heart failure
Selected forms of heart failure are attributed to genetic factors. At least 20% of the cases of heart failure are thought to have directly to an inherited genetic defects (Zhao, et al 2017). The dystrophin gene is linked to x-linked cardiomyopathy heart failure.in addition, familial cardiomyopathy is linked to gene mutations such as the B-myosin heavy chain, cardio troponin- T and α – tropomyosin, myosin –binding protein C and myosin light chains 1 and 2 (Heinemann&Vogel 2016). However, innovative programs are being pursued in order to take the full advantage of the current knowledge of the relationship of the genetics and a heart disease. Research is underway to map all forms of inherited cardiomyopathy and provides the most accurate prognostic information and assists in planning therapeutic programs. In addition, the emphasis is on introducing genes in myocyte to facilitate the cell division in order to replace damaged myocardium with new myocytes (Fitchet, et al 2016)
Nonpharmacological HF Intervention Strategies
Diet and nutrition
Patients diagnosed with heart failure control the amount of salt in their food. The recommended salt content is less than 2000mg. These patients also have the fluid restriction of 1500ml-2000ml. In this case, the salt substitute is advised although it must also be used with caution as they may contain some elements of potassium. In cases of alcoholic cardiomyopathy, alcohol consumption is not allowed. In special cases, alcohol intake is allowed.in addition, it is commendable for these patients to incorporate weight reduction strategy by avoiding foods that contain high contents of cholesterol and other fats. The body max index should be less than 25 (Kanda,et al 2017). This will assist in preventing the cases of cardiac cachexia and malnutrition.
Rest and exercise
Traditionally, patients diagnosed with heart failure were instructed not to perform any exercise to avoid the ailment deterioration. However, recent studies have shown that physical exercise mitigates the effects of acute heart failure if the patient is in a stable condition, the patient is advised to undertake daily physical exercises, but it’s also advisable for the patient to follow the physical exercise instructions from the physician. (Hinton &Ware 2017) In addition, the exercise training decreases the circulation of catecholamine levels, and oxidative effects, and increase nitric oxide which led to minimized peripheral vasoconstriction, improved endothelial function, and enhanced endothelial repair. Physical exercises also combat muscle wasting and restore the catabolic imbalance. There is a significant evidence that training programs in HF patients are safe and they induce favorable clinical effects (Zaidi& Brueckner 2017).
The Improved symptom recognition and self-care behavior.
Patients and their partners have a right to information in regard to HF symptoms, this will assist patients to promptly identify deterioration and apply the relevant strategy in case of an exacerbation. In addition, patients are supposed to weigh on a regular basis, so that unexpected weight gain can be addressed in time. In this case, patients are encouraged to monitor other probable symptoms and note the changes. Physicians have an important role to play in creating awareness of the seriousness of these symptoms and the appropriate actions to take (Frestad& Prescott 2017).In addition other self-care measures to These includes discouraging smoking for patients who are diagnosed with HF, immunization of influenza and pneumococcal as this may reduce infections of respiratory system, stress reduction therapies are also advised for reduction of anxiety to in patients suffering from HF (Thiene, Corrado & Basso 2016.)
In conclusion, our comprehension of the pathophysiology of heart failure is important in recent advances in the therapeutic management in this discipline. The pathophysiology of the failure of the cardiac system has unfolded over the last 30 years. New strategies and advances have yielded positive therapeutic changes. However, the newest research has found the mechanism that contributes to the advancement of a heart failure. Thereby, mitigating the negative effects of the cardiac failure. This is done through an alteration of the molecular level changes in the myocyte and on the prevention of cellular morphologic However, future therapies of mitigating on heart failure will likely encompass multifaceted framework to the multiple and complicated components that contribute to the progression of the disease. Through research, some significant advances have been made in elucidating the genetic factors that contribute the onset and the progression of the HF. In addition, further study is needed to establish the patients who are at risk and ultimately engage more protective therapies. Therefore, new innovations in long-term interventions and development of extensive medical therapies that slow or reverse the cardiac system failure are generally helping to curb the heart failure thereby illuminating our vision for the future.
Bibliography
Asgar, A.W., Mack, M.J. and Stone, G.W., 2015. Secondary mitral regurgitation in heart failure: pathophysiology, prognosis, and therapeutic considerations. Journal of the American College of Cardiology, 65(12), pp.1231-1248.
Azad, N. and Lemay, G., 2014. Management of chronic heart failure in the older population. Journal of geriatric cardiology: JGC, 11(4), p.329.
Basuray, A., French, B., Ky, B., Vorovich, E., Olt, C., Sweitzer, N.K., Cappola, T.P. and Fang, J.C., 2014. Heart failure with recovered ejection fraction: clinical description, biomarkers, and outcomes. Circulation, pp.CIRCULATIONAHA-113.
Clark, A.L., Fonarow, G.C. and Horwich, T.B., 2014. Obesity and the obesity paradox in heart failure. Progress in cardiovascular diseases, 56(4), pp.409-414.
Cruz, D.N., Schmidt-Ott, K.M., Vescovo, G., House, A.A., Kellum, J.A., Ronco, C., McCullough, P.A. and Acute Dialysis Quality Initiative, 2013. Pathophysiology of cardiorenal syndrome type 2 in stable chronic heart failure: workgroup statements from the eleventh consensus conference of the Acute Dialysis Quality Initiative (ADQI). In ADQI Consensus on AKI Biomarkers and Cardiorenal Syndromes (Vol. 182, pp. 117-136). Karger Publishers.
Desai, A.S., McMurray, J.J., Packer, M., Swedberg, K., Rouleau, J.L., Chen, F., Gong, J., Rizkala, A.R., Brahimi, A., Claggett, B. and Finn, P.V., 2015. Effect of the angiotensin-receptor-neprilysin inhibitor LCZ696 compared with enalapril on mode of death in heart failure patients. European heart journal, 36(30), pp.1990-1997.
Doehner, W., Frenneaux, M. and Anker, S.D., 2014. Metabolic impairment in heart failure. Journal of the American College of Cardiology, 64(13), pp.1388-1400.
Eckel, R.H., Jakicic, J.M., Ard, J.D., De Jesus, J.M., Miller, N.H., Hubbard, V.S., Lee, I.M., Lichtenstein, A.H., Loria, C.M., Millen, B.E. and Nonas, C.A., 2014. 2013 AHA/ACC guideline on lifestyle management to reduce cardiovascular risk: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology, 63(25 Part B), pp.2960-2984.
Fitchett, D., Zinman, B., Wanner, C., Lachin, J.M., Hantel, S., Salsali, A., Johansen, O.E., Woerle, H.J., Broedl, U.C. and Inzucchi, S.E., 2016. Heart failure outcomes with empagliflozin in patients with type 2 diabetes at high cardiovascular risk: results of the EMPA-REG OUTCOME® trial. European heart journal, 37(19), pp.1526-1534.
Florea, V.G. and Cohn, J.N., 2014. The autonomic nervous system and heart failure. Circulation research, 114(11), pp.1815-1826.
Frestad, D. and Prescott, E., 2017. Vital exhaustion and coronary heart disease risk: a systematic review and meta-analysis. Psychosomatic medicine, 79(3), pp.260-272.
Heinemann, A. and Vogel, H., 2016. Anatomy of the Heart and Lungs in Postmortem Angiography. In Atlas of Postmortem Angiography (pp. 179-196). Springer International Publishing
Hinton, R.B. and Ware, S.M., 2017. Heart failure in pediatric patients with congenital heart disease. Circulation research, 120(6), pp.978-994.
Kanda, T., Fujita, M., Iida, O., Masuda, M., Okamoto, S., Ishihara, T., Nanto, K., Tsujimura, T., Sunaga, A., Uematsu, M. and Mano, T., 2017. P3367A novel index of left ventricular stiffness predicting clinical outcome in patients with heart failure. European Heart Journal, 38(suppl_1).
Lymperopoulos, A., Rengo, G. and Koch, W.J., 2013. Adrenergic nervous system in heart failure. Circulation research, 113(6), pp.739-753.
Mann, D.L. and Felker, G.M., 2014. Heart Failure E-Book: A Companion to Braunwald’s Heart Disease. Elsevier Health Sciences.
Ponikowski, P., Anker, S.D., AlHabib, K.F., Cowie, M.R., Force, T.L., Hu, S., Jaarsma, T., Krum, H., Rastogi, V., Rohde, L.E. and Samal, U.C., 2014. Heart failure: preventing disease and death worldwide. ESC Heart Failure, 1(1), pp.4-25.
Roger, V.L., 2013. Epidemiology of heart failure. Circulation research, 113(6), pp.646-659.
Sacks, F.M., Lichtenstein, A.H., Wu, J.H., Appel, L.J., Creager, M.A., Kris-Etherton, P.M., Miller, M., Rimm, E.B., Rudel, L.L., Robinson, J.G. and Stone, N.J., 2017. Dietary fats and cardiovascular disease: a presidential advisory from the American Heart Association. Circulation, 136(3), pp.e1-e23.
Segura, A.M., Frazier, O.H. and Buja, L.M., 2014. Fibrosis and heart failure. Heart failure reviews, 19(2), pp.173-185.
Senni, M., Paulus, W.J., Gavazzi, A., Fraser, A.G., Díez, J., Solomon, S.D., Smiseth, O.A., Guazzi, M., Lam, C.S., Maggioni, A.P. and Tschöpe, C., 2014. New strategies for heart failure with preserved ejection fraction: the importance of targeted therapies for heart failure phenotypes. European heart journal, 35(40), pp.2797-2815.
Tham, Y.K., Bernardo, B.C., Ooi, J.Y., Weeks, K.L. and McMullen, J.R., 2015. Pathophysiology of cardiac hypertrophy and heart failure: signaling pathways and novel therapeutic targets. Archives of toxicology, 89(9), pp.1401-1438.
Thiene, G., Corrado, D. and Basso, C., 2016. Coronary Artery Disease. In Sudden Cardiac Death in the Young and Athletes (pp. 21-71). Springer Milan.
Yancy, C.W., Jessup, M., Bozkurt, B., Butler, J., Casey, D.E., Drazner, M.H., Fonarow, G.C., Geraci, S.A., Horwich, T., Januzzi, J.L. and Johnson, M.R., 2013. 2013 ACCF/AHA guideline for the management of heart failure. Circulation, pp.CIR-0b013e31829e8776.
Zaidi, S. and Brueckner, M., 2017. Genetics and genomics of congenital heart disease. Circulation research, 120(6), pp.923-940.
Zhao, M., Vaartjes, I., Graham, I., Grobbee, D., Spiering, W., Klipstein-Grobusch, K., Woodward, M. and Peters, S.A., 2017. Sex differences in risk factor management of coronary heart disease across three regions. Heart, 103(20), pp.1587-1594.