Heart failure – an update [autosaved]

Editor's Notes

• #6: Dr. (Name) says: Heart failure is a disease that reduces the heart’s ability to pump blood. To give you a better idea of what happens during heart failure, I’m first going to show you a normal heart. Click on the animation: In a normal heart, the blood is pumped in a smooth and synchronized way. (Explain the flow patterns to and from the right and left heart if you wish.) In a normal heart, the heart pumps enough blood to match the body’s need for oxygen. Discuss “plumbing” functions and “electrical” functions.
• #9: Some of the information we gathered was very interesting…..
• #10: The figure shows the average length of hospital admission by main diagnosis in NHS hospitals in England for 2000/01. Petersen S, Rayner M, Wolstenholme J. Coronary heart disease statistics: heart failure supplement. London: British Heart Foundation, 2002.
• #14: Dr. (Name) says: Short explanation of the diagnostic process – what might take place during each test. Discuss commonly done tests including the role of the echocardiogram .
• #16: Let’s compare our heart to this donkey, and our body to the wagon that this donkey has to pull every day. A healthy heart is like an energetic donkey, which without fatigue, pulls the wagon full of weights. Conversely, a diseased heart will have difficulty meeting metabolic demands (or pulling the wagon).
• #21: As previously seen, there are many causes of heart failure. Some diseases, however, tend to more adversely affect the heart’s systolic function (ventricular contraction/ejection), while others tend to more adversely affect diastolic function (ventricular filling/relaxation). This provides a useful way of classifying heart failure from a hemodynamic standpoint. Most patients who have systolic dysfunction also have a component of diastolic dysfunction.
• #22: Systolic and Diastolic Dysfunction Diastolic dysfunction caused by compromise myocardial relaxation in the presence of myocardial contractility and ejection fraction. One third to one half of patients with heart failure have normal ventricular contractile function, and are said to have diastolic heart failure. Abnormal diastolic function may be due to impaired early relaxation, increased stiffness of the ventricle, or both. Diastolic dysfunction results in impairment in ventricular filling. LV end-diastolic pressures are elevated, leading to pulmonary venous congestion. Diastolic dysfunction is most commonly associated with left ventricular hypertrophy (LVH) due to hypertension, and occurs frequently in elderly women. Increased resistance to filling results from the increased LV mass itself, and also from interstitial fibrosis and subendocardial ischemia. Diastolic dysfunction can occur in the absence of LVH due to ischemia, myocardial infiltration (e.g., amyloidosis), or pericardial constriction. Systolic Heart Failure Most commonly, heart failure reflects an abnormality of ventricular contractile function. End-systolic volume, end-diastolic volume, and end-diastolic pressure are increased, and stroke volume falls. Symptoms of reduced cardiac output (e.g., fatigue) develop. In addition, increased LV end-diastolic pressure is transmitted back to the pulmonary veins, resulting in transudation of fluid into the pulmonary interstitium and symptoms of pulmonary congestion. The most common cause of contractile dysfunction is loss of myocytes due to myocardial infarction. Other causes of systolic heart failure include dilated cardiomyopathy, myocarditis, and chronic alcohol use. The most common form of heart failure , that due to coronary artery disease, often reflects a combination of systolic and diastolic dysfunction. Systolic dysfunction is due to prior infarction and ischemia-induced decrease in contractility. Diastolic dysfunction is due to chronic replacement fibrosis and ischemia-induced decrease in distensibility.
• #23: Mixed systolic and diastolic failure Disease states as dilated cardiomyopathy (DCM), poor EFs (<35%), high pulmonary pressures Biventricula r failure (both ventricles may be dilated, poor filling and emptying capacity)
• #29: The other mechanism in the neurohumoral response to heart failure is the renin-angiotensin-aldosterone system (RAAS). In the RAAS, Renin ( secreted by the kidney ) acts on Angiotensinogen (secreted by the liver) to make Angiotensin I. The Angiotensin converting enzyme (secreted by the lungs) acts on Angiotensin I to make Angiotensin II. Angiotensin II in turn causes vasoconstriction, an increase in aldosterone, facilitates the release of norepinephrine from the SNS, causes sodium reabsorption, stimulates vasopressin secretion from the brain (discussed later), and increases contractility. Subsequently, remodeling of the heart occurs. In a heart failure patient, the effects of Angiotensin II are not beneficial. Why not think about using a medication to block the conversion of Angiotensin I to II? Or, an agent that blocks the Angiotensin I receptor? These blocking agents will be discussed later when we talk about the treatment of heart failure.
• #30: Consensus- COOPERATIVE NORTH SCANDINAVIAN ENALAPRIL SURVIVAL STUDY pt were already taking digoxin and diuretics. Subsequent SOLVD- STUDIES OF LEFT VENTRICULAR DYSFUNCTION- Proved consensus at a earlier stage of heart failure even asymptomatic
• #32: ARBs are comparable to ACE-I in reduction all-cause mortality and heart failure-related hospitalizations in patients with NYHA classes II and III heart failure.
• #33: Adding an ARB to ACE-inhibitor therapy provides further mortality benfit in slected patients. In this trial of patients with NYHA classes II to IV heart failure, candesartan added to existing ACE-I therapy reduced cardiovasular death (NNT, 28 over 3.5 years) and reduced heart-failure related hospital admission. A second study found no benefit
• #34: POTENTIAL CONCERNS REGARDING INITIATION OF β BLOCKERS BEFORE DISCHARGE The 1999 guidelines of the Heart Failure Society of America suggested that, to maximize safety, there should be a period of clinical stability while on standard therapy before instituting β blockers and that initiation in patients who have HF requires a careful baseline evaluation of clinical status. 26 Because it is based on early, large-scale trials in which patients who had chronic HF were treated with standard therapy consisting of ACE inhibitors, digoxin, and a diuretic for ≥2 months before starting β-blocker therapy, this recommendation led to many HF clinicians postponing β-blocker therapy for ≥2 to 4 weeks until stability had been achieved. This plays into the concern many practitioners have that beginning β blockade in patients who have HF will necessarily worsen HF during the titration period. In the Randomized Evaluation of Strategies for Left Ventricular Dysfunction, there was a significantly larger number of hospitalizations for worsening HF with controlled-release metoprolol than with placebo (p = 0.026). However, there was also a 54% lower risk of death with controlled-release metoprolol (p = 0.057) and a significant increase in LV ejection fraction (p = 0.001). 2 , 27 In the COPERNICUS study, there were significantly fewer patients who used carvedilol and then developed serious adverse events than those who used placebo (p <0.002). 10 This trial showed that the adverse event of utmost concern to clinicians regarding the initiation of β blockers, i.e., worsening HF, occurred less frequently with carvedilol than with placebo. 10 , 28 The COPERNICUS, in effect, indicated that the early initiation of life-saving therapies should be approached with a sense of urgency and provides a mandate for expediting the administration of β-blocker therapy in patients who have HF. After comparing initiation before and after discharge with respect to tolerability and safety in the IMPACT-HF study, it was found that there were no significant differences between groups in the occurrence of serious adverse events (bradycardia, hypotension, and worsening HF) or the occurrence of these events leading to the permanent withdrawal of the β blocker. Fewer patients developed worsening of HF before than after discharge (0.5% vs 1.7%), and there was a lower composite rate of death and rehospitalization. 25 These major trials clearly refute the common practices and perceptions regarding β-blocker therapy for HF that lead to unnecessary delays in treatment and deny patients established benefits of this therapy. Specifically, the results of these studies challenge the beliefs commonly held by many clinicians that initiation of β blockade is characterized by an unfavorable benefit/risk ratio, that survival curves do not diverge in favor of β blockers for many months, and that early initiation necessarily carries the risk of worsening HF or intolerance that leads to withdrawal of treatment. Rather, these studies clearly demonstrate the high degree of tolerability for β blockers and that there is a lower relative rate of discontinuation with β blockers than with placebo. Several β blockers, e.g., atenolol, timolol, and propranolol, have proven efficacy as secondary prevention after myocardial infarction but not as therapy for HF. Among those agents that have established efficacy in HF, e.g., carvedilol, bisoprolol, and metoprolol, there are pharmacologic differences that may alter the clinical responses to these agents in HF 24 and may have an affect on in-hospital initiation of therapy. The β-1–specific blockers may decrease cardiac output, increase vascular resistance, or decrease renal blood flow, all of which can contribute to worsening HF. 30 The β blockers with an α blockade, such as carvedilol, increase cardiac output and decrease vascular resistance. The vasodilatory activity due to α-1 blockade offsets myocardial depression due to β blockade, and the broad-based sympathetic antagonism may protect the patient against worsening HF in the early stages of initiation. 30 In the MERIT-HF trial of patients who had HF of New York Heart Association classes III and IV, a decrease in the mortality rate was observed with the use of metoprolol, a β-1–specific blocker; however, the metoprolol-treated group had a higher rate (8.1%) of withdrawal in the first 90 days than did the placebo-treated group (5.9%). 31 Data from COPERNICUS trial showed that the carvedilol-treated group had a lower rate of worsening HF (5.1%) than did the placebo group (6.4%) during the initiation phase. 25 In the IMPACT-HF study, only 0.5% of patients withdrew due to worsening HF if they had been initiated with carvedilol before discharge versus 1.7% of patients who had been initiated with a β blocker of the physician's choice after discharge. 25 Therefore, these considerations may make carvedilol a better agent for initiating β-blocker therapy in the hospital setting.
• #35: 6 RCT’s that included more than 9,000 patients already taking ACE-I showed a significant reduction in total mortality and sudden dearth (NNT 24, and #% over 1-2 years) Carvedilol or Metoprolol European Trial 2003 In a recent trial , patient with NYHA classes II to IV heart failure who were treated with carvedilol had greater reductions in mortality (NNT, 18 over 5 years) and cardiovascular mortality (NNT, 16 over five years) than those treated with metoprolol but, hypotension was more common among the carvedilol group (14 versus 11 percent) Bisoprolol and metoprolol are b1-selective with no vasodilating properties Coreg- is alpha 1 beta 1 and beta 2 with vasoldilating properties
• #37: Add aldactone in moderate to severe heart failure, favorable effects on LV remodeling Randomized Aldactone RALES-survival benefit of spironolactone in patient with severe heart failure and favorable effexts on LV remodeling Most common risk is hyperkalemia and 10 % of men will experinece breast pain an gynecomastia Eplerenone-newer more selective aldosterone inhibitor has been shown to reduce all-cause mortality following myocardial infraction with Left ventricular dysfunction (NNT, 43 for 16 months) Has not yet been studied in patient with CHF who have not yet had a MI
• #38: Patients taking digoxin are less lekely to be hospitalized for worseing heart failrue (NNT, 27 to 115 over three years) and their heart failure symptoms may worsen if digoxin is withdrawn Positive inotrope with autonomic effects: increased parasympathetic tone DIG Trial (Garg R et al. N Engl J Med 1997;336:525-33.) : 6,800 pts w/ EF < 45% randomized to digoxin vs. placebo (Background tx: ACEI, diuretic) No difference in mortality between two groups 25% reduction in CV death or hospitalization for HF (p<0.001) 28% reduction in hospitalization for HF (p<0.001) Toxicity: renal dysfunction, elderly
• #40: $530/dy Decreased 30 days survival Side effect of hypotension No benefit as an outpatient basis
• #45: Many patients with advanced systolic heart failure exhibit significant inter- or intraventricular conduction delays that disturb the synchronous beating of the left and right ventricles so that they pump less efficiently. This delayed ventricular activation and contraction is referred to as ventricular dysynchrony and is easily recognized by a wide QRS complex on an ECG. This IVCD (inter- or intraventricular conduction delay) typically has left bundle branch morphology.
• #48: Dr. (Name) says: Sudden Cardiac Arrest is as scary as it sounds. It means that your heart suddenly starts beating very fast and quivers instead of beating in a regular and organized way. No blood gets pumped, and you will die unless you get treatment within minutes. We’ll talk more about treatments in a moment. Unlike a heart attack, SCA is caused by an electrical problem in your heart. SCA can strike without warning, and there are no symptoms.
• #49: Click on animation. Dr. (Name) says: Some people with Class III and IV heart failure can benefit from a heart failure pacemaker that can help your heart beat more efficiently by coordinating or synchronizing the way the heart beats, so your heart pumps more efficiently. It works by automatically checking your heart function 24 hours a day. This type of heart device is also called cardiac resynchronization therapy or CRT. You may also hear the term biventricular pacing. All refer to the same kind of treatment. Treatment with a heart device may make you feel better. Although many people experience dramatic improvements in their quality of life and in their heart failure symptoms, results may vary. Not everyone responds to the treatment in the same way. It is also important to note that heart failure pacemakers do not cure heart failure--a heart failure pacemaker is part of an overall treatment plan. Describe heart failure pacemaker device: A heart failure pacemaker is about the size of a small pocket watch that contains a battery and computer circuitry to correct your heart rhythm and help your heart beat more efficiently. Small insulated wires called leads connect the device to the heart. We’re going to pass around a plastic replica of a Medtronic combination heart failure pacemaker and defibrillator pacemaker . Facilitators circulate and pass around replicas and collect them. Before I move on, I’d like to say a few words about Medtronic, the company helping us put on the seminar today. Medtronic was the first company to introduce a pacemaker in the United States. Physicians worldwide have prescribed heart failure pacemakers for more than 120,000 patients. Other people with heart failure are in danger of having heartbeats that are irregular and/or too fast. These irregular heart beats can cause you to feel short of breath and light headed. Such episodes may also be life threatening if not treated quickly. Some heart devices also contain a defibrillator in addition to the special kind of pacemaker. This combination device also sends out small electrical signals to restore your normal heart rhythm. If the small signals do not work, the device sends out a shock to reset your heart rhythm. This kind of device is also used to treat SCA.
• #61: Looking at demographics nation-wide… Currently 12% of our pop is over the age of 65, by 2030 it is expected to be at about 20%
• #62: Keeping that recommendation in mind, the HVHC HF Task force was created. It’s purpose was to…..
• #64: Patients are screened for the Telehealth program…..some may refuse