Diagnóstico da ICC

Evaluation of the patient with suspected heart failure
Author
Wilson S Colucci, MD
Section Editor
Stephen S Gottlieb, MD
Deputy Editor
Susan B Yeon, MD, JD, FACC

INTRODUCTION — Heart failure (HF) is a common clinical syndrome caused by a variety of cardiac diseases [1]. The initial evaluation of the patient with suspected HF due to systolic or diastolic dysfunction will be reviewed here. Evaluation of the etiology and management of HF and evaluation and treatment of acute decompensated HF are discussed separately.

DEFINITION — Heart failure (HF) is a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood. It is characterized by specific symptoms, such as dyspnea and fatigue, and signs, such as those related to fluid retention. There are many ways to assess cardiac function. However, there is no diagnostic test for HF, since it is largely a clinical diagnosis that is based upon a careful history and physical examination (table 1).

CLINICAL PRESENTATION — The approach to the patient with suspected HF includes the history and physical examination, and diagnostic tests to help establish the diagnosis, assess acuity and severity and initiate assessment of etiology. Recommendations for the evaluation of patients with HF were included in the 2005 American College of Cardiology (ACC/AHA) guidelines with 2009 focused update (algorithm 1) [2], the 2010 Heart Failure Society of America (HFSA) guidelines [3], the 2008 European Society of Cardiology (ESC) guidelines [4], and the 2006 Canadian Cardiovascular Society (CCS) consensus conference [5].

The discussion below focuses on diagnosis of heart failure. The history and physical examination of the patient with suspected heart failure should also include assessment of risk factors and potential etiologies of heart failure as discussed separately.
Physical examination — The physical examination can provide evidence of the presence and extent of cardiac filling pressure elevation, volume overload, ventricular enlargement, pulmonary hypertension, and reduction in cardiac output.

In the study of primary care patients cited above, the physical finding of a displaced apical impulse had the best combination of sensitivity, specificity, and positive and negative predictive value of any physical sign of systolic HF [8]. Other strong predictors of HF included a gallop rhythm and elevated jugular venous pressure.

Vital signs and appearance — Patients with advanced HF may show evidence of a major decline in cardiac output and therefore a decrease in tissue perfusion. Four major findings suggest severity of the cardiac dysfunction: resting sinus tachycardia, narrow pulse pressure, diaphoresis, and peripheral vasoconstriction. The last abnormality is manifested as cool, pale, and sometimes cyanotic extremities (due to the combination of decreased perfusion and increased oxygen extraction). A decrease in cardiac output should be suspected when the pulse pressure is reduced below 25 mmHg.

Both the cardiac disease itself and the secondary neurohumoral adaptation contribute to the low output state. Patients compensate for a fall in cardiac output by increasing sympathetic outflow with resultant shunting of the cardiac output to vital organs.

An irregularly irregular pulse is suggestive of atrial fibrillation which frequently accompanies HF.
Volume assessment — There are three major manifestations of volume overload in patients with HF: pulmonary congestion, peripheral edema, and elevated jugular venous pressure.

Pulmonary congestion that may manifest as rales is more prominent in acute or subacute disease. As noted above, chronic HF is associated with increases in venous capacitance and lymphatic drainage of the lungs; as a result, rales are often absent even though the pulmonary capillary pressure is elevated. Continued sodium retention in this setting preferentially accumulates in the periphery although a chronic elevation in pulmonary venous pressure can lead to pleural effusions.

Peripheral edema is manifested by swelling of the legs (which is more prominent when the patient is upright), and may also cause ascites, scrotal edema, hepatomegaly, and splenomegaly [9]. (See "Approach to the adult patient with splenomegaly and other splenic disorders".) In this setting, manual compression of the right upper quadrant to increase venous return may elevate jugular venous pressure above the transient 1 to 3 cm elevations seen in normal individuals. This sign is known as the hepatojugular reflux. (See "Examination of the jugular venous pulse", section on 'Hepatojugular reflux'.)

Elevated jugular venous pressure is usually present if peripheral edema is due to HF, since it is the high intracapillary pressure that is responsible for fluid movement into the interstitium. With the patient sitting at 45º jugular venous pressure can be estimated from the height above the left atrium of venous pulsations in the internal jugular vein. The height of external jugular vein pulsations may also be helpful but care must be taken to avoid spurious interpretation. (See "Examination of the jugular venous pulse".)

The accuracy of clinical volume assessment is discussed below. (See 'Diagnostic accuracy of clinical features' below.)

Pulsus alternans — Pulsus alternans, if present, is virtually pathognomonic of severe left ventricular failure. This phenomenon is characterized by evenly spaced alternating strong and weak peripheral pulses. It is best appreciated by applying light pressure on the peripheral arterial pulse, and can be confirmed by measuring the blood pressure. When the cuff pressure is slowly released, phase I Korotkoff sounds are initially heard only during the alternate strong beats; with further release of cuff pressure, the softer sounds of the weak beat also appear. The degree of pulsus alternans can be quantitated by measuring the difference in systolic pressure between the strong and the weak beat. (See "Examination of the arterial pulse", section on 'Pulsus alternans'.)

The pathophysiology of pulsus alternans is not well understood. The severe ventricular dysfunction may be associated with variations in contractility secondary to shifts in afterload, preload, and electrical excitability [10].

Precordial palpation — Ventricular chamber size can be estimated by precordial palpation. An apical impulse that is laterally displaced past the midclavicular line is usually indicative of left ventricular enlargement. Left ventricular dysfunction can also lead to sustained apical impulse, which may be accompanied by a parasternal lift in the setting of right ventricular hypertrophy or enlargement. The S3 may be palpable in severe ventricular failure. (See "Examination of the precordial pulsation".)

Heart sounds — An S3 gallop is associated with left atrial pressures exceeding 20 mmHg, increased left ventricular end-diastolic pressures (>15 mmHg), and elevated serum brain natriuretic peptide concentrations. However, there is appreciable interobserver variability in the ability to detect an S3 that cannot be solely explained by the experience of the observer [11,12]. In addition, in a phonocardiographic study of patients who were undergoing cardiac catheterization, an S3 was not very sensitive (40 to 50 percent) for the detection of an elevated left ventricular end-diastolic pressure or a reduced left ventricular ejection fraction; however, the S3 was highly specific (90 percent) for these parameters and for an elevated serum brain natriuretic peptide concentration [13]. Similarly, an S3 (or “extra heart sound”) has a low sensitivity (eg, 4 to 11 percent) but high specificity (eg, 99 percent) for clinical diagnosis of HF [6,7]. (See "Auscultation of heart sounds", section on 'Left ventricular gallops'.)

Pulmonary hypertension — Patients with chronic HF often develop secondary pulmonary hypertension, which can contribute to dyspnea as pulmonary pressures rise with exertion. These patients may also complain of substernal chest pressure, typical of angina. In this setting, elevated right ventricular end-diastolic pressure leads to secondary right ventricular subendocardial ischemia. Physical signs of pulmonary hypertension can include increased intensity of P2, a murmur of pulmonary insufficiency, a parasternal lift, and a palpable pulmonic tap (felt in the left second intercostal space). (See "Auscultation of cardiac murmurs" and "Auscultation of heart sounds" and "Examination of the precordial pulsation".)

Diagnostic accuracy of clinical features — The accuracy of symptoms and signs for the clinical diagnosis of heart failure was evaluated by a systematic review that included data from 15 studies of patients with suspected heart failure [6]:  

Dyspnea was the only symptom or sign with high sensitivity (87 percent) but its specificity was low (51 percent).
Other clinical features had relatively high specificity but low sensitivity:
Symptoms - Orthopnea (specificity and sensitivity of 89 and 44 percent) and history of myocardial infarction (89 and 26 percent).
Signs - Extra heart sounds were highly specific (99 percent) but had low sensitivity (11 percent). In this population, hepatomegaly was also highly specific (97 percent) but had low sensitivity (17 percent). Greater specificity than sensitivity was also seen for cardiomegaly (85 and 27 percent), lung crepitation (81 and 51 percent), edema (72 and 53 percent), and elevated jugular venous pressure (70 and 52 percent).  
The accuracy of clinical evaluation of cardiac filling pressures varies among observers as illustrated by a study of 116 patients undergoing cardiac catheterization [14]. Signs of elevated right heart filling pressure included increased jugular venous pressure, peripheral edema, and ascites. Signs of elevated left heart filling pressure included findings of elevated right heart filling pressure as well as gallops or rales.

Right and left heart filling pressures were accurately estimated by physical examination in 71 and 60 percent of 215 observations. Examination by staff cardiologists was more accurate than by trainees for right heart pressures (82 versus 67 percent) and left heart pressures (71 versus 55 percent).
Exposure to echocardiographic and NT-pro-BNP results did not improve the accuracy of clinical evaluations. The accuracy of estimation of right filling pressure by echocardiographic examination of the IVC (75 percent) was similar to the accuracy of physical examination. The accuracy of estimates of left heart filling pressures by NT-pro-BNP (67 percent) and by echocardiography E/e’ ratio (60 percent) was also similar to physical examination. (See 'NT-proBNP' below and "Natriuretic peptide measurement in heart failure" and "Echocardiographic evaluation of left ventricular diastolic function", section on 'Algorithms for estimating LV filling pressure'.)
The diagnosis of HF is based upon a constellation of symptoms, signs, and test results. Diagnostic rules based upon combinations of clinical features are discussed below (See 'Diagnostic rules' below.).

DIFFERENTIAL DIAGNOSIS — Many of the symptoms and signs of HF are non-specific so other potential causes should be considered. Patients with HF may present with a syndrome of decreased exercise tolerance, fluid retention, or both [2]. Various other causes for such symptoms and signs should also be considered.

Patients with decreased exercise tolerance have symptoms of dyspnea or fatigue with exertion and may also have symptoms at rest. Heart failure should be distinguished from other causes of dyspnea including myocardial ischemia, pulmonary disease, and other disorders [15]. Causes of fatigue include deconditioning, sleep apnea and depression. (See "Approach to the patient with dyspnea" and "Approach to the adult patient with fatigue".)

For example, chronic obstructive pulmonary disease (COPD) and HF may be difficult to distinguish in some patients. Because of the high prevalence of these disorders, their similar presentations, and their frequent coexistence, it is reasonable to consider both diagnoses, not only in patients presenting with dyspnea for the first time, but also in any patient with one of these diagnoses who presents with a deterioration in respiratory status [16]. This issue is discussed in detail separately. (See "Chronic obstructive pulmonary disease: Definition, clinical manifestations, diagnosis, and staging", section on 'Diagnosis' and "Chronic obstructive pulmonary disease: Definition, clinical manifestations, diagnosis, and staging".)
Patients presenting with fluid retention may complain of leg or abdominal swelling. Heart failure should be distinguished from other causes of edema including venous thrombosis or insufficiency, renal sodium retention, drug side effect (eg, calcium channel blocker) and cirrhosis. (See "Clinical manifestations and diagnosis of edema in adults" and "Pathophysiology and etiology of edema in adults".)
INITIAL TESTING

Electrocardiogram — Most patients with HF due to systolic dysfunction have a significant abnormality on an electrocardiogram (ECG). A normal ECG makes systolic dysfunction unlikely (98 percent negative predictive value) [17].

Although the ECG may be less predictive of HF than the BNP (or NT-proBNP) level [6], the ECG may show findings that favor the presence of a specific cause of HF and can also detect arrhythmias (eg, atrial fibrillation) that suggest heart disease and may cause or exacerbate HF. (See "Tachycardia-mediated cardiomyopathy" and "Evaluation of the patient with heart failure or cardiomyopathy".)

The ECG is particularly important for identifying evidence of acute or prior myocardial infarction or acute ischemia. Ischemia may cause symptoms of dyspnea similar to HF and may also cause or exacerbate HF. (See "Electrocardiogram in the diagnosis of myocardial ischemia and infarction".)

Initial blood tests — Recommended initial blood tests for patients with symptoms and signs of HF include:

A complete blood count which may suggest concurrent or alternate conditions. Anemia or infection can exacerbate pre-existing HF. (See "Impact of anemia in patients with heart failure".)
Serum electrolytes, blood urea nitrogen, and creatinine may indicate associated conditions. Hyponatremia generally indicates severe HF, though it may occasionally result from excessive diuresis [2]. Renal impairment may be caused by and/or contribute to HF exacerbation. Baseline evaluation of electrolytes and creatine is also necessary when initiating therapy with diuretics and/or angiotensin converting enzyme inhibitors.
Liver function tests, which may be affected by hepatic congestion. In one study, gamma-glutamyltransferase level (GGT) >2 times the upper limit of normal was the only standard initial blood test that added diagnostic value to the history and physical examination [7]. However, NT-proBNP was the most powerful supplementary test.
Fasting blood glucose to detect underlying diabetes mellitus. (See "Heart failure in diabetes mellitus".)
BNP and NT-proBNP — Brain natriuretic peptide (BNP) is a natriuretic hormone released primarily from the heart, particularly the ventricles. The active BNP hormone is cleaved from the C-terminal end of its prohormone, pro-BNP. The N-terminal fragment (NT-proBNP) is also released into the circulation. The plasma concentrations of BNP and NT-proBNP are increased in patients with left ventricular dysfunction, particularly those with heart failure.

BNP or NT-proBNP levels are useful in distinguishing HF due to systolic and/or diastolic dysfunction from other causes of dyspnea. As noted below, studies developing and validating diagnostic rules for HF have found that the BNP or NT-proBNP levels add greater diagnostic value to the history and physical examination than other initial tests (ECG, chest x-ray, and initial blood tests) [6,7]. Evidence of efficacy and limitations of BNP and NT-proBNP levels in the diagnosis of HF is discussed in detail separately. (See "Natriuretic peptide measurement in heart failure".)

Measurement of plasma BNP or NT-proBNP is suggested in the evaluation of patients with suspected HF when the diagnosis is uncertain, as recommended in the 2005 ACC/AHA guidelines with 2009 update as well as the 2006 HFSA, 2008 ESC, and 2006 CCS guidelines [2,4,5,15]. Elevated natriuretic peptide levels should be interpreted in the context of other clinical information; they may lend weight to the diagnosis of HF or trigger consideration of HF but should NOT be used in isolation to diagnose HF [2].

BNP — Most dyspneic patients with HF have values above 400 pg/mL, while values below 100 pg/mL have a very high negative predictive value for HF as a cause of dyspnea [18]. In the range between 100 and 400 pg/mL, plasma BNP concentrations are not very sensitive or specific for detecting or excluding HF. Other diagnoses, such as pulmonary embolism, LV dysfunction without exacerbation, and cor pulmonale should also be considered in patients with plasma BNP concentrations in this range.

Atrial fibrillation (AF) is associated with higher levels of BNP in the absence of HF. In one analysis, a BNP cutoff of ≥100 pg/mL was associated with a specificity of only 40 percent compared to 79 percent in patients without AF [19]. Using a cutoff of ≥200 pg/mL in patients with AF increased specificity from 40 to 73 percent with a smaller reduction in sensitivity from 95 to 85 percent.

Normal plasma BNP values increase with age and are higher in women than men [20]. Thus, somewhat higher cutoff values may be needed in these settings, although the optimal discriminatory values that should be used have not been determined.

NT-proBNP — In normal subjects, the plasma concentrations of BNP and NT-proBNP are similar (approximately 10 pmol/L). However, in patients with LV dysfunction, plasma NT-proBNP concentrations are approximately fourfold higher than BNP concentrations [21]. (See "Natriuretic peptide measurement in heart failure", section on 'Plasma N-terminal pro-BNP'.)

The optimal values for distinguishing HF from other causes of dyspnea vary with patient age. In a large multicenter study, for patients <50, 50 to 75, and >75 years of age, the optimal plasma NT-proBNP cutoffs for diagnosing HF were 450 pg/mL, 900 pg/mL, and 1800 pg/mL respectively [22]. Overall, these cutoffs yielded a sensitivity and specificity of 90 and 84 percent, respectively. Across the entire population, NT-proBNP levels below 300 pg/mL were optimal for excluding a diagnosis of HF, with a negative predictive value of 98 percent.

Limitations of BNP and NT-proBNP — There are several important limitations to the use of plasma BNP and NT-proBNP for diagnosis of HF [23]:

Patients may present with more than one cause of dyspnea (such as pneumonia and an exacerbation of HF). Thus, a high plasma BNP or NT-proBNP concentration does not exclude the presence of other diseases.
In some patients with acute decompensated HF, plasma BNP or NT-proBNP levels are not diagnostic.
Some patients with severe chronic HF may have persistently elevated plasma BNP or NT-proBNP concentrations regardless of treatment, and such levels may not be useful in guiding management.
Right heart failure and pulmonary hypertension are associated with elevations in plasma BNP and NT-proBNP. However, when right heart failure is due solely to lung disease and not due to secondary pulmonary hypertension from left sided heart disease or as part of a global cardiomyopathy, elevated plasma BNP may be misinterpreted since dyspnea in these patients is due to lung disease not left heart failure.
Plasma BNP and NT-proBNP levels tend to be lower in obese patients and are elevated in patients with renal failure, and some acute noncardiac illnesses such as sepsis. Greater increases in NT-proBNP than BNP levels are observed in renal failure.
Measurement and interpretation of BNP and NT-proBNP levels is discussed in detail separately. (See "Natriuretic peptide measurement in heart failure".)

Chest x-ray — The chest x-ray is a useful first diagnostic test, particularly in the evaluation of patients who present with dyspnea, to differentiate HF from primary pulmonary disease [24-26]. Findings suggestive of HF include cardiomegaly (cardiac-to-thoracic width ratio above 50 percent), cephalization of the pulmonary vessels, Kerley B-lines, and pleural effusions (image 1A-E). The cardiac size and silhouette may also reveal signs of congenital anomalies (ventricular or atrial septal defect) or valvular disease (mitral stenosis or aortic stenosis).

A systematic review of the utility of the chest x-ray to diagnose LV dysfunction concluded that redistribution and cardiomegaly were the best predictors of increased preload and reduced ejection fraction, respectively [25]. Neither finding, however, was sufficient to make a definitive diagnosis of HF. In a multicenter study of 880 patients, alveolar edema, interstitial edema, and cephalization all had a specificity of >90 percent for HF, but only cardiomegaly had a sensitivity >50 percent [26].

Diagnostic accuracy of initial testing — The accuracy of initial testing for the clinical diagnosis of heart failure was evaluated by a systematic review that included data from 15 studies of patients with suspected heart failure [6]:

BNP or NT-proBNP levels have relatively high sensitivity (both 93 percent) and more limited specificity for clinical diagnosis of HF (74 and 65 percent). (See "Natriuretic peptide measurement in heart failure".)
As noted above, an ECG has relatively high sensitivity (89 percent) but more limited specificity (56 percent). (See 'Electrocardiogram' above.)
Chest x-ray evidence of HF is helpful in confirming the diagnosis since it has relatively high specificity (83 percent) though more limited sensitivity (68 percent).  
Diagnostic rules for HF that include initial testing are discussed below. (See 'Diagnostic rules' below.)

ECHOCARDIOGRAPHY — In patients with symptoms and signs of HF, echocardiography is helpful for determining whether ventricular function and hemodynamics are consistent with HF and in identifying a cause. The 2007 ACCF/ASE/ACEP/ANC/SCAI/SCCT/SCMR appropriateness criteria rate echocardiography as appropriate in patients with symptoms (including dyspnea, shortness of breath and others) due to a suspected cardiac etiology [27]. They also rate echocardiography appropriate when other studies (such as chest x-ray or elevation of serum BNP) are concerning for cardiac disease.

Important echocardiographic findings include the following:

Atrial and ventricular sizes, which may be helpful in identifying the cause and chronicity of disease. For example, patients with idiopathic dilated cardiomyopathy typically have both left and right atrial and ventricular enlargement (four chamber dilatation) with decreased left systolic ventricular function (image 2 and figure 1 and movie 1 and movie 2 and movie 3). (See "Echocardiographic recognition of cardiomyopathies".)
Global left and right ventricular systolic function (left and right ventricular ejection fraction, LVEF and RVEF). (See "Noninvasive methods for measurement of left ventricular systolic function", section on 'Echocardiography'.)
Diastolic left ventricular function. (See "Echocardiographic evaluation of left ventricular diastolic function".)
Regional wall motion abnormalities in a coronary distribution are suggestive of coronary heart disease but segmental abnormalities also occur commonly in patients with dilated cardiomyopathy
Pericardial disease includes thickening suggestive of constrictive pericarditis or effusion which may or may not be associated with tamponade. (See "Constrictive pericarditis" and "Cardiac tamponade".)
Valvular heart disease
Echocardiography also provides a noninvasive assessment of hemodynamic status:

The pulmonary capillary wedge pressure (PCWP) can be estimated via the ratio (E/Ea or E/E') of tissue Doppler of early mitral inflow velocity (E) to early diastolic velocity of the mitral annulus (Ea or e'). An E/e' ratio >15 suggests a PCWP >15 mm Hg when e' is the mean of medial and lateral mitral annulus early diastolic velocities. Use and limitations of this method are discussed separately. (See "Echocardiographic evaluation of left ventricular diastolic function", section on 'Tissue Doppler imaging'.)
Right ventricular and pulmonary artery pressures can be estimated by the peak velocity of tricuspid regurgitation on Doppler echocardiography. Right atrial pressure may be estimated from evaluating the size of the inferior vena cava and its respiratory variation.
The cardiac output can be estimated by pulsed-wave Doppler from the left ventricular outflow tract [28].
DIAGNOSTIC RULES — Diagnostic rules have been developed in an attempt to increase the accuracy and efficiency of HF diagnosis as illustrated by the following two examples.

An individual patient data analysis tested various diagnostic models in one dataset [6]. The model with the best fit was simplified into the following clinical prediction rule:

Echocardiography is recommended for a patient with suspected HF presenting with symptoms such as breathlessness if any one of the following is present: history of myocardial infarction, or basal crepitations (rales), or male with ankle edema.
A patient with suspected HF without one of the above features is referred for BNP or NT-proBNP level testing. Echocardiography is recommended in the following settings :
Female without ankle edema if BNP >210 to 360 pg/mL (or NT-proBNP >620 to 1060 pg/mL) depending upon local availability of echocardiography.
Male without ankle edema if BNP >130 to 220 pg/mL (or NT-proBNP >390 to 660 pg/mL).
Female with ankle edema if BNP >100 to 180 pg/mL (or NTproBNP >190 to 520 pg/mL).
The above model was applied to other datasets with an area under the ROC curve (AUC) of 0.84 to 0.96. (See "Evaluating diagnostic tests", section on 'Receiver operating characteristic curves'.)

A multicenter prospective study of 721 patients with suspected HF evaluated various models including elements from history, physical examination, and initial testing [7]. A diagnostic rule was developed with the following elements:

Age <60 years (no points), 60 to 70 (4 points), 70 to 80 (7 points), >80 (10 points)
History of myocardial infarction, coronary artery bypass graft surgery, or percutaneous coronary intervention (15 points if present)
Loop diuretic (10 points if present)
Displaced apical impulse (20 points if present)
Rales (14 points if present)
Irregularly irregular pulse (11 points if present)
Heart murmur (10 points if present)
Pulse rate [(bpm-60)/3 points}
Elevated jugular venous pressure (12 points if present)
NT-proBNP (pg/mL) <100 (no points), 100 to 200 (8 points), 200 to 400 (16 points), 400 to 800 (24 points), 800 to 1600 (32 points), 1600 to 3200 (40 points), >3200 (48 points)
With a summed score <13 points, the estimated probability of HF is <10 percent. With a summed score >54 points, the estimated probability of HF is >70 percent. The rule was applied to two external validation datasets with AUC of 0.88 to 0.95. (See "Evaluating diagnostic tests", section on 'Receiver operating characteristic curves'.)

Although both of the above rules performed well when applied to validation datasets, their generalizability to various clinical settings is uncertain.

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)

Basics topic (see "Patient information: Heart failure (The Basics)")
Beyond the Basics topic (see "Patient information: Heart failure (Beyond the Basics)"









Cardiomiopatia lateral:




Raio x normal:




Referência: Uptodate.com


Atualização da Diretriz Brasileira de Insuficiência Cardíaca Crônica - 2012

Métodos Diagnósticos
2.1.1. Eletrocardiograma
Recentemente se demonstrou que escore eletrocardiográfico tem correlação positiva com fibrose miocárdica e correlação
negativa com a fração de ejeção de ventrículo esquerdo (FEVE) em pacientes com cardiomiopatia chagásica14. Também a
variabilidade de amplitude da onda T em pacientes chagásicos foi relacionada a pior prognóstico15.
2.1.2 Troponina e Polimorfismo
Nos últimos anos, a detecção de troponina e sua magnitude têm sido motivo de investigação no cenário da
IC crônica, sendo verificado valor na avaliação de injúria miocárdica mesmo subclínica, e também estratificação
prognóstica16. Limitações quanto à sensibilidade motivaram o desenvolvimento de método mais acurado, como a troponina
ultrassensível, que em estudos iniciais tem demonstrado sua importância especialmente quando comparado à troponina
sérica convencional17. Ensaios futuros relevantes devem definir sua real indicação e importância na prática clínica. Certos
polimorfismos da metaloproteinases podem estar associados a maior incidência de doença isquêmica e melhor prognóstico18.
2.1.3. BNP/NTproBNP
Nas situações em que há dúvida no diagnóstico da IC de FE reduzida e IC de FE preservada (ICFEP), a dosagem do pepídeo
natriurético do tipo B (BNP) pode ser útil para o diagnóstico de congestão pulmonar. Em metanálise recentemente publicada,
a adição da dosagem de BNP ao exame clínico aumentou a acurácia diagnóstica19. Portanto, nas situações de dúvida, o
BNP pode ser utilizado, somado ao exame clínico. Os valores de corte para IC crônica não foram especificamente estudados.
Nos casos de pacientes sem história de infarto do miocárdio ou ECG normal, pode ser realizado antes do ecocardiograma,
segundo análises de custo-efetividade20. A dosagem de BNP no líquido pleural pode ser útil para diagnóstico de derrame
pleural devido a IC21. Na doença de Chagas, BNP e peptídeo natriurético atrial (ANP) têm valor prognóstico e podem estar
elevados em pacientes assintomáticos22.
2.1.4. Ecodopplercardiograma
Reavaliação ecocardiográfica periódica não deve ser procedimento de rotina em pacientes estáveis. Pode ter
utilidade clínica em pacientes que apresentam piora clínica evidente, visando readequar manejo terapêutico. Neste
contexto, informações úteis são: piora de parâmetros de função ventricular esquerda e direita, estimativas
hemodinâmicas e surgimento de valvulopatias funcionais.
2.1.5. Imagem por Medicina Nuclear - SPECT e PET
Os resultados do estudo STICH, comparando os desfechos clínicos em função da presença ou não de viabilidade através de
SPECT ou ecocardiografia de estresse arrefeceram o entusiasmo com a sua pesquisa sistemática, uma vez que a melhora com a
revascularização, nesse estudo, foi independente da presença de viabilidade, pesquisada por esses métodos23. Dúvidas persistem
se os resultados teriam sido diferentes caso o método de pesquisa de viabilidade tivesse sido PET ou ressonância cardíaca.
2.1.6. Tomografia Computadorizada Cardíaca e Ressonância Magnética (Tabelas 3 e 4)
A angiotomografia coronária permite excluir de forma não invasiva a presença de doença arterial coronariana
significativa, principalmente em pacientes de baixo risco ou risco intermediário24. Esse método pode ser utilizado ainda para
avaliar a função ventricular, direita e esquerda, quando outras metodologias não estão disponíveis (portadores de marca-passo
ou janela ecocardiográfica inadequada).
2.1.7. Teste Ergoespirométrico
Diante da estabilidade clínica e sem contraindicações ao exercício, indica-se preferencialmente para avaliação
do paciente o teste de esforço ergoespirométrico ou alternativamente o teste de caminhada de 6 minutos usual ou
monitorizado25, ou o teste ergométrico26,27. Sabe-se que o uso de betabloqueador (BB) reduz a frequência cardíaca máxima durante exercício28. Com a utilização de BB, o valor de consumo máximo de oxigênio durante exercício (VO2) de 10-12,5 ml/kg/
min e a inclinação da relação VE/VCO2 > 35 parecem separar pacientes com IC quanto ao prognóstico.










Referencia: Bocchi EA, Marcondes-Braga FG, Bacal F, Ferraz AS, Albuquerque D, Rodrigues D, et al. Sociedade Brasileira
de Cardiologia. Atualização da Diretriz Brasileira de Insuficiência Cardíaca Crônica - 2012. Arq Bras Cardiol
2012: 98(1 supl. 1): 1-33
http://publicacoes.cardiol.br/consenso/2012/Diretriz%20IC%20Cr%C3%B4nica.pdf