DOCSLIB.ORG

Pathophysiology of Heart Failure Following Myocardial Infarction

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Pathophysiology of Heart Failure Following Myocardial Infarction ii14 Pathophysiology of heart failure following myocardial Heart: first published as 10.1136/hrt.2005.062034 on 14 April 2005. Downloaded from infarction A D Struthers ............................................................................................................................... Heart 2005;91(Suppl II):ii14–ii16. doi: 10.1136/hrt.2005.062034 The structural and functional abnormalities that lead to endothelial dysfunction, identified as a notably reduced vascular response to acetylcholine.3 cardiac death are coronary artery disease and left Heymes and colleagues have reported research ventricular abnormalities related to remodelling (left with transgenic mice that over express aldoster- ventricular hypertrophy, left ventricular systolic dysfunction, one synthase in the myocardium. They found that the transgenic animals had normal cardiac and left ventricular fibrosis). Aldosterone adversely affects function but major coronary artery dysfunction, all of these processes. It produces both a vasculopathy and which for some reason was more pronounced in left ventricular dysfunction and fibrosis. Endothelial males.4 The human and transgenic animal data there- dysfunction in the coronary arteries can lead to acute fore both indicate that aldosterone produces coronary events. Left ventricular dysfunction will cause the endothelial dysfunction. The mechanism is progression of heart failure, and left ventricular fibrosis thought to involve reduction in vascular nitric oxide by increased production of superoxide and dysfunction provide an arrhythmic substrate. The anions. Superoxide anions degrade the nitric combination of acute coronary events and arrhythmias can oxide that is produced by healthy endothelium. lead to sudden cardiac deaths, while acceleration of the Experiments in hyperlipidaemic rabbits have shown a 2.3-fold increase in superoxide anion heart failure disease process can lead to deaths from generation that was reversed when the animals progressive heart failure. The increased understanding of were given aldosterone blockade.5 the mechanistic role of aldosterone in cardiovascular Animal studies have suggested an inflamma- tory component to aldosterone induced vasculo- disease provides a rationale for the positive results that pathy. Administration of aldosterone to rats has have been seen in clinical trials of aldosterone blockade. been shown to be associated with macrophage and monocyte infiltration (a measure of inflam- ........................................................................... http://heart.bmj.com/ mation) within and around the coronary artery wall.6 Other inflammatory signals were also he structural and functional abnormalities demonstrated, with both vascular cell adhesion that lead to cardiac death are coronary artery molecule-1 (VCAM-1) and cyclo-oxygenase-2 disease and left ventricular abnormalities (COX-2) being produced in the coronary T 6 related to remodelling (left ventricular hypertro- arteries. phy, left ventricular systolic dysfunction, and left All of this work suggests that a vasculopathy ventricular fibrosis). Aldosterone is adversely of some kind is produced by aldosterone and, at involved in all of these processes. least in animals, this appears to have an on September 27, 2021 by guest. Protected copyright. inflammatory component. VASCULAR EFFECTS OF ALDOSTERONE Aldosterone produces a vasculopathy that EFFECT OF ALDOSTERONE ON appears to affect the coronary arteries. ANGIOTENSIN Endothelial function has been measured in the Another vascular effect of aldosterone is that it brachial artery of patients with heart failure, appears to be able to feedback on the rest of the with the response to acetylcholine being taken as renin–angiotensin system and to amplify the production of angiotensin II from angiotensin I a measure of the health of the endothelium.1 In (fig 1). If this positive feedback loop is true, it patients given aldosterone blockade there was suggests that administration of an aldosterone an approximate doubling in the forearm blood blocking drug will not only block the effects of flow response to acetylcholine. Aldosterone aldosterone but as a ‘‘byproduct’’ it will also blockade also increased the vascular response produce some additional ACE inhibition, by to N-monomethyl-L-arginine (L-NMMA). blocking the conversion of angiotensin I to A study in patients with mild heart failure who angiotensin II. were already taking a b blocker, statin, and This is something of a pharmacological curio- ....................... angiotensin converting enzyme (ACE) inhibitor sity at present but there are some supporting has also demonstrated that in the presence of 7 Correspondence to: data. In the early 1990s, Sun et al showed in Professor Allan D Struthers, aldosterone blockade there was an improvement Division of Medicine and in acetylcholine mediated, endothelium depen- Therapeutics, Ninewells dent vasodilation.2 It has also been shown that Abbreviations: ACE, angiotensin converting enzyme; COX-2, cyclo-oxygenase- 2; L-NMMA, N-monomethyl-L- Hospital, Dundee DD1 infusion of aldosterone for one hour in healthy 9SY, UK; a.d.struthers@ arginine; MI, myocardial infarction; PIII NP, procollagen dundee.ac.uk individuals (in a dose that does not change the type III amino terminal peptide; VCAM-1, vascular cell ....................... haemodynamics) leads to development of adhesion molecule-1 www.heartjnl.com Pathophysiology of heart failure following MI ii15 Renin Figure 1 Aldosterone is thought Placebo to amplify production of Aldosterone blockade Heart: first published as 10.1136/hrt.2005.062034 on 14 April 2005. Downloaded from angiotensin II from angiotensin I and hence aldosterone blockade p = 0.036 p = 0.006 Angiotensin I produces some ‘‘extra’’ ACE 130 6.0 inhibition. (+) 125 5.5 120 Angiotensin II 2 115 5.0 cm g/m 110 4.5 Aldosterone 105 100 4.0 LV mass index LVIDd animal experiments that aldosterone significantly increased Figure 3 In patients with heart failure, left ventricular mass index and the binding density of ACE receptors, while Ullian et al8 left ventricular internal diastolic diameter were both improved by showed that aldosterone increases angiotensin II receptor aldosterone blockade, indicating that treatment can reduce left 2 number. More recently, researchers in Japan9 have shown ventricular remodelling (MacDonald et al ). that the addition of aldosterone to cultured rat cardiomyo- cytes led to a dramatic 23-fold increase in production of ACE and brought back to control level when the animals were messenger RNA. The effect of aldosterone was time and dose given the aldosterone antagonist eplerenone (fig 2). Similar dependent, and it was significantly inhibited by administra- effects have also been seen outside the heart: in sponta- tion of the aldosterone antagonist spironolactone. neously hypertensive rats, cerebral tissue injury appeared to These in vitro studies indicate that some ACE inhibition be notably reduced by administration of eplerenone at a dose may be occurring with aldosterone blockers and a clinical that did not affect the blood pressure.10 study that we carried out showed similar effects.1 Forearm Suzuki and colleagues reported experiments investigating blood flow response to angiotensin I and II was measured the effect of three months’ treatment with eplerenone on the after one month’s treatment with spironolactone or placebo. progression of left ventricular dysfunction and remodelling in The vascular response to angiotensin I was blunted in the dogs with chronic heart failure induced by intracoronary presence of aldosterone blockade, suggesting that less angio- microembolisations that were discontinued when left ven- tensin I was being converted to angiotensin II, since vaso- tricular ejection fraction was between 30–40%.11 The differ- constriction only occurs on the conversion to angiotensin II. ence between the eplerenone group and a control group in There is therefore a developing body of evidence that there left ventricular end diastolic pressure, left ventricular end is some feedback amplification and that aldosterone block- diastolic volume, and end diastolic wall stress—parameters of ade, in addition to its other benefits, produces some ‘‘extra’’ left ventricular remodelling—were all significant and ACE inhibition. favoured eplerenone, indicating that aldosterone blockade can reduce myocardial remodelling and reduce wall stress after induction of heart failure. http://heart.bmj.com/ ALDOSTERONE AND LEFT VENTRICULAR In a clinical study in patients with mild heart failure,2 left ABNORMALITIES ventricular mass index (a measure of hypertrophy) and left Studies investigating the effects of aldosterone on left ventricular internal diastolic diameter were both improved by ventricular abnormalities have shown a consistent pattern. aldosterone blockade with spironolactone, providing further It appears that aldosterone is able to produce tissue injury, evidence that aldosterone blockade reduces left ventricular including injury to the myocardium, the consequences of remodelling (fig 3). An Italian study has produced similar which include left ventricular dysfunction and left ventri- findings, with reported improvement in both left ventricular cular fibrosis. ejection fraction and maximum oxygen consumption in on September 27, 2021 by guest. Protected copyright. Animal studies have provided evidence that aldosterone patients with chronic heart failure given aldosterone block- blockade can prevent aldosterone induced myocardial injury.
Load more

Recommended publications
  • The Pulmonary Manifestations of Left Heart Failure*
    The Pulmonary Manifestations of Left Heart Failure* Brian K. Gehlbach, MD; and Eugene Geppert, MD Determining whether a patient’s symptoms are the result of heart or lung disease requires an understanding of the influence of pulmonary venous hypertension on lung function. Herein, we describe the effects of acute and chronic elevations of pulmonary venous pressure on the mechanical and gas-exchanging properties of the lung. The mechanisms responsible for various symptoms of congestive heart failure are described, and the significance of sleep-disordered breathing in patients with heart disease is considered. While the initial clinical evaluation of patients with dyspnea is imprecise, measurement of B-type natriuretic peptide levels may prove useful in this setting. (CHEST 2004; 125:669–682) Key words: Cheyne-Stokes respiration; congestive heart failure; differential diagnosis; dyspnea; pulmonary edema; respiratory function tests; sleep apnea syndromes Abbreviations: CHF ϭ congestive heart failure; CSR-CSA ϭ Cheyne-Stokes respiration with central sleep apnea; CPAP ϭ continuous positive airway pressure; Dlco ϭ diffusing capacity of the lung for carbon monoxide; DM ϭ membrane conductance; FRC ϭ functional residual capacity; OSA ϭ obstructive sleep apnea; TLC ϭ total lung ϭ ˙ ˙ ϭ capacity; VC capillary volume; Ve/Vco2 ventilatory equivalent for carbon dioxide early 5 million Americans have congestive heart For a detailed review of the pathophysiology of N failure (CHF), with 400,000 new cases diag- high-pressure pulmonary edema, the reader is re- nosed each year.1 Unfortunately, despite the consid- ferred to several excellent recent reviews.2–4 erable progress that has been made in understanding the pathophysiology of pulmonary edema, the pul- monary complications of this condition continue to The Pathophysiology of Pulmonary challenge the bedside clinician.
    [Show full text]
  • Cardiovascular Disease and Rehab
    EXERCISE AND CARDIOVASCULAR ! CARDIOVASCULAR DISEASE Exercise plays a significant role in the prevention and rehabilitation of cardiovascular diseases. High blood pressure, high cholesterol, diabetes and obesity can all be positively affected by an appropriate and regular exercise program which in turn benefits cardiovascular health. Cardiovascular disease can come in many forms including: Acute coronary syndromes (coronary artery disease), myocardial ischemia, myocardial infarction (MI), Peripheral artery disease and more. Exercise can improve cardiovascular endurance and can improve overall quality of life. If you have had a cardiac event and are ready to start an appropriate exercise plan, Cardiac Rehabilitation may be the best option for you. Please call 317-745-3580 (Danville Hospital campus), 317-718-2454 (YMCA Avon campus) or 317-456-9058 (Brownsburg Hospital campus) for more information. SAFETY PRECAUTIONS • Ask your healthcare team which activities are most appropriate for you. • If prescribed nitroglycerine, always carry it with you especially during exercise and take all other medications as prescribed. • Start slow and gradually progress. If active before event, fitness levels may be significantly lower – listen to your body. A longer cool down may reduce complications. • Stop exercising immediately if you experience chest pain, fatigue, or labored breathing. • Avoid exercising in extreme weather conditions. • Drink plenty of water before, during, and after exercise. • Wear a medical identification bracelet, necklace, or ID tag in case of emergency. • Wear proper fitting shoes and socks, and check feet after exercise. STANDARD GUIDELINES F – 3-5 days a week. Include low weight resistance training 2 days/week I – 40-80% of exercise capacity using the heart rate reserve (HRR) (220-age=HRmax; HRmax-HRrest = HRR) T – 20-60mins/session, may start with sessions of 5-15 mins if necessary T – Large rhythmic muscle group activities that are low impact (walking, swimming, biking) Get wellness tips to keep YOU healthy at HENDRICKS.ORG/SOCIAL..
    [Show full text]
  • Percutaneous Mitral Valve Therapies: State of the Art in 2020 LA ACP Annual Meeting
    Percutaneous Mitral Valve Therapies: State of the Art in 2020 LA ACP Annual Meeting Steven R Bailey MD MSCAI, FACC, FAHA,FACP Professor and Chair, Department of Medicine Malcolm Feist Chair of Interventional Cardiology LSU Health Shreveport Professor Emeritus, UH Health San Antonio [email protected] SRB March 2020 Disclosure Statement of Financial Interest Within the past 12 months, I or my spouse/partner have had a financial interest/arrangement or affiliation with the organization(s) listed below. Affiliation/Financial Relationship Company • Grant/Research Support • None • Consulting Fees/Honoraria • BSCI, Abbot DSMB • Intellectual Property Rights • UTHSCSA • Other Financial Benefit • CCI Editor In Chief SRB March 2020 The 30,000 Ft View Maria SRB March 2020 SRB March 2020 Mitral Stenosis • The most common etiology of MS is rheumatic fever, with a latency of approximately 10 to 20 years after the initial streptococcal infection. Symptoms usually appear in adulthood • Other etiologies are rare but include: congenital MS radiation exposure atrial myxoma mucopolysaccharidoses • MS secondary to calcific annular disease is increasingly seen in elderly patients, and in patients with advanced chronic kidney disease. SRB March 2020 Mitral Stenosis • Mitral stenosis most commonly results from rheumatic heart disease fusion of the valve leaflet cusps at the commissures thickening and shortening of the chordae calcium deposition within the valve leaflets • Characteristic “fish-mouth” or “hockey stick” appearance on the echocardiogram (depending on view) SRB March 2020 Mitral Stenosis: Natural History • The severity of symptoms depends primarily on the degree of stenosis. • Symptoms often go unrecognized by patient and physician until significant shortness of breath, hemoptysis, or atrial fibrillation develops.
    [Show full text]
  • Myocardial Infarction (Heart Attack)
    Sacramento Heart & Vascular Medical Associates February 19, 2012 500 University Ave. Sacramento, CA 95825 Page 1 916-830-2000 Fax: 916-830-2001 Patient Information For: Only A Test Myocardial Infarction (Heart Attack) What is a myocardial infarction (MI)? Myocardial infarction (MI) is a heart attack. It happens when blood flow to a part of the heart is suddenly blocked. How does it occur? Myocardial infarction may occur at any time and often occurs without warning. As we grow older, our coronary arteries may become narrowed by the buildup of cholesterol plaque. When the arteries narrow, less blood can go through them, and less oxygen gets to the heart muscle. The process of narrowing is called atherosclerosis. The narrower the artery becomes, the more likely it is that a blood clot may form and block the artery completely, causing a heart attack. Sometimes sudden blockages can occur even in places where the artery was not narrow before. A heart attack may also occur when the heart muscle needs more oxygen than the blood vessels can provide. This might happen, for example, during hard exercise such as shoveling snow, or with a sudden increase in blood pressure. Less commonly, a heart attack can occur due to coronary spasm. Coronary spasm is a sudden and temporary narrowing of a small part of an artery that supplies blood to the heart. It may be caused by smoking or drugs such as cocaine. Risk factors for heart disease include: - cigarette smoking - a family history of heart attack - diabetes - overweight - high blood pressure - high blood cholesterol - low HDL cholesterol (that is, too little "good" cholesterol) - stress - a lifestyle that does not include much physical activity.
    [Show full text]
  • Currentstateofknowledgeonaetiol
    European Heart Journal (2013) 34, 2636–2648 ESC REPORT doi:10.1093/eurheartj/eht210 Current state of knowledge on aetiology, diagnosis, management, and therapy of myocarditis: a position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases Downloaded from Alida L. P. Caforio1†*, Sabine Pankuweit2†, Eloisa Arbustini3, Cristina Basso4, Juan Gimeno-Blanes5,StephanB.Felix6,MichaelFu7,TiinaHelio¨ 8, Stephane Heymans9, http://eurheartj.oxfordjournals.org/ Roland Jahns10,KarinKlingel11, Ales Linhart12, Bernhard Maisch2, William McKenna13, Jens Mogensen14, Yigal M. Pinto15,ArsenRistic16, Heinz-Peter Schultheiss17, Hubert Seggewiss18, Luigi Tavazzi19,GaetanoThiene4,AliYilmaz20, Philippe Charron21,andPerryM.Elliott13 1Division of Cardiology, Department of Cardiological Thoracic and Vascular Sciences, University of Padua, Padova, Italy; 2Universita¨tsklinikum Gießen und Marburg GmbH, Standort Marburg, Klinik fu¨r Kardiologie, Marburg, Germany; 3Academic Hospital IRCCS Foundation Policlinico, San Matteo, Pavia, Italy; 4Cardiovascular Pathology, Department of Cardiological Thoracic and Vascular Sciences, University of Padua, Padova, Italy; 5Servicio de Cardiologia, Hospital U. Virgen de Arrixaca Ctra. Murcia-Cartagena s/n, El Palmar, Spain; 6Medizinische Klinik B, University of Greifswald, Greifswald, Germany; 7Department of Medicine, Heart Failure Unit, Sahlgrenska Hospital, University of Go¨teborg, Go¨teborg, Sweden; 8Division of Cardiology, Helsinki University Central Hospital, Heart & Lung Centre,
    [Show full text]
  • The Management of Acute Coronary Syndromes in Patients Presenting
    CONCISE GUIDANCE Clinical Medicine 2021 Vol 21, No 2: e206–11 The management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: key points from the ESC 2020 Clinical Practice Guidelines for the general and emergency physician Authors: Ramesh NadarajahA and Chris GaleB There have been significant advances in the diagnosis and international decline in mortality rates.2,3 In September 2020, management of non-ST-segment elevation myocardial the European Society of Cardiology (ESC) published updated infarction over recent years, which has been reflected in an Clinical Practice Guidelines for the management of ACS in patients international decline in mortality rates. This article provides an presenting without persistent ST-segment elevation,4 5 years after overview of the 2020 European Society of Cardiology Clinical the last iteration. ABSTRACT Practice Guidelines for the topic, concentrating on areas relevant The guidelines stipulate a number of updated recommendations to the general or emergency physician. The recommendations (supplementary material S1). The strength of a recommendation and underlying evidence basis are analysed in three key and level of evidence used to justify it are weighted and graded areas: diagnosis (the recommendation to use high sensitivity according to predefined scales (Table 1). This focused review troponin and how to apply it), pathways (the recommendation provides learning points derived from the guidelines in areas to facilitate early invasive coronary angiography to improve relevant to general and emergency physicians, including diagnosis outcomes and shorten hospital stays) and treatment (a (recommendation to use high sensitivity troponin), pathways paradigm shift in the use of early intensive platelet inhibition).
    [Show full text]
  • Heart Failure
    FACT SHEET FOR PATIENTS AND FAMILIES Heart Failure What is it? Enlarged heart Heart failure is a condition in which your heart can’t pump enough blood to meet your body’s needs. Usually, this is because your heart muscle is too weak to “squeeze” out enough blood with each beat. But heart failure can also happen when your heart gets stiff “Normal” heart and can’t fill up with enough blood between each beat. Heart failure is found most often in older people, but it can happen to anyone at any age. It’s a serious condition — and also quite common. Many people with heart failure continue to have a full and active life for many years after their diagnosis. What are the symptoms? Symptoms of heart failure vary based on the type of With heart failure, initial damage weakens the heart failure you have. Common symptoms include: heart muscle. This makes your heart beat faster, and the muscle stretches or thickens. Over time, • Shortness of breath the heart muscle begins to wear out. • Cough • Feeling very tired and weak • Atherosclerosis (coronary artery disease). • Weight gain (from fluid buildup) Atherosclerosis is when the arteries that supply your • Swollen ankles, feet, belly, lower back, and fingers heart with blood become narrowed by fatty plaque • Puffiness or swelling around the eyes buildup. This restricts the amount of oxygen your • Trouble concentrating or remembering heart gets and weakens the muscle. It can also cause a heart attack, which can damage your heart even more. The main cause of heart failure (heart muscle damage and weakness) cannot be cured, but symptoms can be • High blood pressure (hypertension).
    [Show full text]
  • Heart Disease and Diseases of the Circulatory System in Westchester
    Westchester County 2016.01 Department of Health KEEP HEALTHY @wchealthdept AND Community Health Assessment Data Update GET #keephealthy THE STATS Heart Disease and Diseases of the Circulatory System in Westchester In this issue: Heart disease as a Heart disease is the number one cause of death in Westchester County. leading cause of death in Westchester county In 2012, heart disease accounted for 2,113 deaths or 31% of all deaths Deaths due to heart disease across different in the county. Adding in 490 deaths due to stroke and other diseases population and risk of the circulatory system, total deaths from circulatory disease are groups 60% higher than the next leading cause of death - cancer. Hospitalizations due to cardiovascular disease- related conditions, Selected Causes of Death in Westchester County, 2012 including diseases of the heart Emergency room visits 2% 3% 7% due to cardiovascular disease-related 3% conditions Selected risk factors 4% that contribute to Heart Disease, cardiovascular disease 4% in Westchester county 31% 5% 9% Cerebrovascular Jiali Li, Ph.D. Director of Disease (Stroke), Research & Evaluation Neoplasms 5% Planning & Evaluation (Cancer), 24% Other Circulatory, Renee Recchia, MPH 3% Acting Deputy Commissioner of Administration Heart Disease Cerebrovascular Disease (Stroke) Project Staff: Other Circulatory Neoplasms (Cancer) Bonnie Lam, MPH Respiratory Diseases External Causes (e.g. accidents) Medical Data Analyst Communicable Diseases Nervous System Diseases Milagros Venuti, MPA Digestive System Diseases
    [Show full text]
  • Treatment of Acute Coronary Syndrome
    Acute Coronary Syndrome: Current Treatment TIMOTHY L. SWITAJ, MD, U.S. Army Medical Department Center and School, Fort Sam Houston, Texas SCOTT R. CHRISTENSEN, MD, Martin Army Community Hospital Family Medicine Residency Program, Fort Benning, Georgia DEAN M. BREWER, DO, Guthrie Ambulatory Health Care Clinic, Fort Drum, New York Acute coronary syndrome continues to be a significant cause of morbidity and mortality in the United States. Family physicians need to identify and mitigate risk factors early, as well as recognize and respond to acute coronary syn- drome events quickly in any clinical setting. Diagnosis can be made based on patient history, symptoms, electrocardi- ography findings, and cardiac biomarkers, which delineate between ST elevation myocardial infarction and non–ST elevation acute coronary syndrome. Rapid reperfusion with primary percutaneous coronary intervention is the goal with either clinical presentation. Coupled with appropriate medical management, percutaneous coronary interven- tion can improve short- and long-term outcomes following myocardial infarction. If percutaneous coronary interven- tion cannot be performed rapidly, patients with ST elevation myocardial infarction can be treated with fibrinolytic therapy. Fibrinolysis is not recommended in patients with non–ST elevation acute coronary syndrome; therefore, these patients should be treated with medical management if they are at low risk of coronary events or if percutaneous coronary intervention cannot be performed. Post–myocardial infarction care should
    [Show full text]
  • Cardiovascular Disease: a Costly Burden for America. Projections
    CARDIOVASCULAR DISEASE: A COSTLY BURDEN FOR AMERICA PROJECTIONS THROUGH 2035 CARDIOVASCULAR DISEASE: A COSTLY BURDEN FOR AMERICA — PROJECTIONS THROUGH 2035 american heart association CVD Burden Report CVD Burden association heart american table of contents INTRODUCTION ...................................................................................5 ABOUT THIS STUDY ................................................................................................... 6 WHAT IS CVD? ......................................................................................................... 6 Atrial Fibrillation Congestive Heart Failure Coronary Heart Disease High Blood Pressure Stroke PROJECTIONS: PREVALENCE OF CVD .............................................................7 Latest Projections Age, Race, Sex – Differences That Matter PROJECTIONS: COSTS OF CVD ................................................................. 8-11 The Cost Generators: Aging Baby Boomers Medical Costs Breakdown Direct Costs + Indirect Costs RECOMMENDATIONS .............................................................................13-14 Research Prevention Affordable Health Care 3 CARDIOVASCULAR DISEASE: A COSTLY BURDEN FOR AMERICA — PROJECTIONS THROUGH 2035 american heart association CVD Burden Report CVD Burden association heart american Introduction Cardiovascular disease (CVD) has been the leading killer In addition, CVD has become our nation’s costliest chronic of Americans for decades. In years past, a heart attack disease. In 2014, stroke and heart
    [Show full text]
  • Heart3-Congestive Heart Failure
    HEART DISEASE Congestive Heart Failure What is congestive heart failure? Congestive Heart Failure (CHF) is a term that refers to the heart’s inability to pump adequate blood to the body. There are many causes of CHF in dogs. The two most common causes are mitral valve insufficiency (MVI) and dilated cardiomyopathy (DCM). Clinical signs vary depending on whether the dog has left- or right-sided heart failure. The most common symptoms are decreased stamina, coughing or difficulty breathing. What is the difference in the signs? Right-sided congestive heart failure causes poor venous return to the heart. In other words, when the heart contracts instead of the right ventricle pushing the blood through the lungs for oxygenation, some returns to the right auricle. This blood is unable to be cleared from the systemic circulation and consequently becomes “congested”. Fluid accumulates in the abdomen and/or the chest cavity, interfering with the function of the organs in these areas. The abdomen may become enlarged with fluid called ascites. Fluid may also leak from veins and swelling may appear in the limbs (peripheral edema). When CHF involves the left ventricle, blood is not pumped into the systemic circulation and builds up in the lungs. Fluid then seeps into the lung tissue resulting in pulmonary edema. This causes coughing and difficulty breathing. Is CHF due mainly to heart valve disease? CHF is most commonly caused by valvular insufficiency. It is estimated that 80% of the canine CHF cases are caused by MVI. However, there are many other causes. Disease of the heart muscle (cardiomyopathy), irregularities of rhythm and narrowing of some of the major blood vessels can also cause CHF.
    [Show full text]
  • Inflammation and Your Heart: Endocarditis, Pericarditis and Myocarditis
    Inflammation and your heart: Endocarditis, pericarditis and myocarditis Types of inflammation Myocarditis When you see the letters ‘itis’ at the end of a What causes myocarditis? Will I need treatment? word, it means inflammation. Myocarditis is inflammation of the myocardium Myocarditis is often mild and goes unnoticed, but – the heart muscle. It is usually caused by a viral, you may need to take medicines to relieve your Myocarditis, pericarditis and bacterial or fungal infection. Sometimes the cause is symptoms such as non-steroidal anti-inflammatories endocarditis refer to inflammation unknown – or ‘idiopathic’. and sometimes antibiotics. around or in the heart. If the myocarditis it is causing a problem with What are the symptoms? how well your heart pumps, you may develop the • Myocarditis – inflammation of the myocardium The symptoms of myocarditis usually include a (the heart muscle) symptoms of heart failure which you will need to pain or tightness in your chest which can spread to take several different types of medicines for. In very • Pericarditis – inflammation of the pericardium other parts of your body, shortness of breath and extreme cases where there is severe damage to the (the sac which surrounds tiredness. You may also have flu like symptoms, such heart you may be considered for a heart transplant. the heart) as a high temperature, feeling tired, headaches and aching muscles and joints. • Endocarditis – inflammation of the Inflammation of the heart often causes chest pain, endocardium (the inner lining of the heart) What tests will I need? and you may feel like you are having a heart attack. If you have not been diagnosed with one of You may need to have an electrocardiogram (ECG), these conditions and you have chest pain, or any echocardiogram (a scan of your heart similar to an of the symptoms we describe below, call 999 ultrasound) and various blood tests.
    [Show full text]