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Systolic and diastolic heart failure: different phenotypes of the same disease?

Traditional pathophysiological concepts of chronic heart failure have largely focused on the haemodynamic consequences of ventricular systolic dysfunction. How these concepts relate to the pathophysiology of diastolic heart failure, i.e., heart failure with a preserved ejection fraction is, however, unclear, causing uncertainty about pathophysiology, diagnosis and management. Recent measurements of regional myocardial systolic function in patients with diastolic heart failure indicate that systolic and diastolic heart failure may be more closely related than previously anticipated. Rather than being considered as separate diseases with a distinct pathophysiology, systolic and diastolic heart failure may be merely different clinical presentations within a phenotypic spectrum of one and the same disease. In this review, we will interpret these new insights in a broader conceptual context of chronic heart failure and design novel paradigms in which systolic and diastolic heart failure jointly progress in a pathophysiological time trajectory of only one disease.

Diastole↗

Clinical features and prognosis associated with a preserved left ventricular systolic function in a large cohort of congestive heart failure outpatients managed by cardiologists. Data from the Italian Network on Congestive Heart Failure.

BACKGROUND: The aim of this study was to evaluate the clinical characteristics, 1-year prognosis and therapeutic approach of heart failure with a preserved left ventricular systolic function in a large multicenter registry of patients referred to specialized heart failure clinics. METHODS: The study population consisted of 5164 outpatients (mean age 62 +/- 12 years, 78.8% male, 28.1% in NYHA functional class III-IV) with an available left ventricular ejection fraction (LVEF) measurement at the initial evaluation for enrollment in the Italian Network on Congestive Heart Failure. A 1-year follow-up was available for 2390 patients. RESULTS: 2859 out of 5164 patients (55.4%) had an LVEF < 35%, 1618 (31.3%) had an LVEF between 35 and 45%, and 687 patients (13.3%) had an LVEF > 45%. Patients with an LVEF > 45% were significantly older, more often female and presented a significantly higher prevalence of a hypertensive etiology, obesity and atrial fibrillation. The severity of the clinical picture, as indicated by a lower prevalence of NYHA class III-IV (17.2 vs 35.6%, p = 0.001) and a third heart sound (14.8 vs 33.5%, p = 0.001), was less in patients with an LVEF > 45%. The therapeutic approach differed significantly, with a larger use of calcium antagonists and beta-blockers in patients with an LVEF > 45%, while ACE-inhibitors, diuretics and digoxin were more often prescribed to those with an impaired LVEF. The 1-year mortality and morbidity (all cause and congestive heart failure worsening hospitalizations) were significantly lower in patients with a preserved left ventricular systolic function compared to those with left ventricular systolic dysfunction (8.9 vs 18.8% for mortality, p = 0.001, and 8.3 vs 16.5% for hospital readmissions due to worsening congestive heart failure, p = 0.001, respectively). CONCLUSIONS: Patients with congestive heart failure and a preserved left ventricular systolic function seem to constitute a distinct population not infrequently presenting even in the clinical setting of specialized heart failure clinics. Further studies are needed to establish a definitive and standardized diagnosis and the most appropriate therapy for congestive heart failure with a normal LVEF.

Aged↗

[Congestive heart failure with intact systolic function].

A retrospective study was undertaken of the cases of patients admitted for congestive cardiac failure over a 4 year period, and investigated by radionuclide angiography to determine the prevalence of cardiac failure with normal left ventricular systolic function, to document the underlying mechanisms of this condition and to assess whether the clinical data could predict the presence or absence of left ventricular systolic dysfunction. After excluding patients with significant valvular disease, severe renal failure, or myocardial infarction in the previous 2 months, the study population comprised 152 patients divided into 2 groups: Group I (N = 112) with abnormal systolic function (radionuclide ejection fraction less than 45%) and Group II (N = 40) with normal systolic function (radionuclide ejection fraction greater than or equal to 45%). The clinical, echocardiographic and radionuclide angiographic data was analysed (global ejection fraction in both groups and peak filling rate in Group II). The patients in Group II (26% of the total study population) were older (66.5 +/- 12.4 vs 61.3 +/- 12.3 years, p less than or equal to 0.02), were more often female (35% vs 17.9%, p less than or equal to 0.02), had acute cardiac failure (75% vs 37%, p less than 0.00001), and were frequently hypertensive (65% vs 39%, p less than or equal to 0.005). Univariate analysis of clinical and radiological signs did not show any significant difference between the two groups except for increased jugular venous pressure and cardiomegaly which were more common in Group I (56% vs 25%, p less than 0.00001 and 93% vs 68%, p less than or equal to 0.00001, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Diastolic function in valvular heart disease.

Diastolic dysfunction in patients with valvular heart disease is characterized by an impaired isovolumic relaxation, a normal or even enhanced early diastolic filling rate and an increased myocardial stiffness. These abnormalities do not depend on coexisting systolic dysfunction but are often combined. Several mechanisms are responsible for the occurrence of diastolic dysfunction, such as increased wall stress, altered myocardial structure, subendocardial hypoperfusion and/or diastolic calcium overload. Postoperative regression of myocardial hypertrophy is beneficial in regard to wall stress, subendocardial hypoperfusion and calcium overload but diastolic dysfunction might become worse after valve replacement due to a relative increase in interstitial fibrosis consequent to the decrease in myocyte mass (= myocardial remodeling). Persisting diastolic dysfunction with a substantial rise in left ventricular filling pressure can be observed during dynamic exercise in postoperative patients with preoperative severe pressure overload hypertrophy. Thus, diastolic dysfunction can be present as a primary derangement of cardiac function and can be unmasked as an abnormal response of diastolic filling pressure during exercise.

Cardiomegaly↗

ACE inhibitor use in elderly patients with systolic left ventricular dysfunction: problems and opportunities.

The ACE inhibitors have been found effective in reducing the morbidity and mortality of both post-infarction patients and those with chronic systolic left ventricular dysfunction. However, their use is limited--particularly in elderly patients because of poor tolerance partly due to bradykinin-induced side-effects such as renal dysfunction, first-dose hypotension, and cough. Thus, the introduction of the angiotensin II type I receptor antagonists--that block the effects of angiotensin II without increasing bradykinin concentration--may be particularly important in the treatment of elderly patients. The role of the angiotensin II type I receptor antagonists in patients with systolic left ventricular dysfunction is currently being explored in direct comparison with and in conjunction with the ACE inhibitors. Furthermore, important questions about the most effective dose of ACE inhibitor and ACE inhibitor use in conjunction with aspirin and the NSAIDs still have to be answered. Thus, although we have learnt much about the role of ACE inhibitors in heart failure treatment, we are still at an early stage in the application of this knowledge, particularly in elderly patients.

Aged↗

Clinical and echocardiographic determinants of ultrasound lung comets.

BACKGROUND: Ultrasound lung comets (ULCs) are an echographic sign of extravascular lung water, that originate from water-thickened interlobular septa. AIM: To establish the echocardiographic correlates of ULCs. METHODS: 340 in-hospital patients (68 +/- 12years, 115 females) admitted to adult cardiology department underwent upon admission a separate evaluation of chest ULCs and a comprehensive 2D and Doppler echocardiography assessment, including the degree of left ventricular diastolic dysfunction (from 0 = normal to 3 = restrictive pattern). A patient ULC score has been obtained by summing the number of ULCs from each of the scanning spaces in the anterior right and left chest, from second to fifth intercostal space. RESULTS: Multivariate linear regression analysis identified New York Heart Association (NYHA) class (OR = 2.1, CI = 1.4-2.9), ejection fraction (OR 0.954, CI = 0.928-0.981) and degree of diastolic dysfunction (OR = 2.438, CI = 1.418-4.190) as the only parameters independently associated to the number of ULCs. CONCLUSION: ULCs are a simple echographic sign of extravascular lung water, more frequently associated with left ventricular diastolic and/or systolic dysfunction. ULCs can usefully integrate the clinical and pathophysiological information provided by conventional 2D and Doppler echocardiography, in patients with known or suspected heart failure and dyspnoea as a presenting symptom.

Aged↗

Prognostic value of left atrial enlargement in patients with idiopathic dilated cardiomyopathy and ischemic cardiomyopathy.

Previous studies have shown that abnormal mitral flow patterns and left atrial (LA) enlargement are independently associated with survival in patients with left ventricular (LV) dysfunction. However, it is not known whether these outcome indicators can provide different information in patients of various age groups. This study was designed to assess the prognostic value of the restrictive mitral flow pattern (RMFP) and increased LA size in patients with LV dysfunction (ejection fraction <45%) grouped into those < or = 70 years old (n = 102; mean age 61) and those >70 years old (n = 105; mean age 78). Echocardiographic and Doppler indexes were recorded in patients with LV systolic dysfunction due to dilated cardiomyopathy who were followed up for 22 plus minus 14 months. In patients >70 years, indexed LA size (>26 mm/m(2)) was the single best predictor of death (hazard ratio [HR] 3.0, p = 0.018) and emerged as the most important outcome variable of the combined end point (HR 2.2, p = 0.016) on multivariate analysis. In patients < or =70 years, RMFP, characterized by an early wave deceleration time <140 ms, was independently associated with cardiac death or heart failure hospitalization (HR 5.7, p = 0.0013). When demographics, clinical, echocardiographic, and Doppler measurements were analyzed in hierarchical order, indexed LA size yielded the most valuable contribution in predicting the combined end point in older patients (global chi-square from 11.5 to 18.7). RMFP was associated with the higher additional prognostic value in younger patients (global chi-square from 14.4 to 24.1). These data suggest that LA enlargement has an independent and additional prognostic value in elderly patients with LV dysfunction.

Aged↗

Is abnormal iodine-123-MIBG kinetics associated with left ventricular dysfunction in patients with diabetes mellitus?

BACKGROUND: Although autonomic neuropathy is frequently recognized in patients with diabetes mellitus, it is uncertain whether cardiac sympathetic neuropathy may play a role in the development of diabetic cardiomyopathy. METHODS AND RESULTS: In 10 control subjects and 61 patients with diabetes mellitus who did not have coronary artery disease, cardiac sympathetic function and left ventricular ejection fraction (LVEF) were evaluated by using iodine-123-metaiodobenzylguanidine (MIBG) imaging and echocardiography, respectively. Dynamic acquisitions and planar images obtained 15 and 150 minutes after injection were used as a means of measuring early and late myocardial uptake and clearance rates of MIBG from the heart. Eight patients with an LVEF less than 50% demonstrated a lower late myocardial MIBG uptake (0.0043% +/- 0.0017% vs. 0.0024% +/- 0.0009%/pixel, P = .002) and a higher clearance rate (22.9% +/- 17.7% vs. 49.3% +/- 12.2%, P<.0001) than the 53 patients with an LVEF of 50% or greater, although the age, sex, type of diabetes mellitus, and frequency of neuropathy, retinopathy, and nephropathy were not significantly different between the 2 subgroups. The LVEF correlated weakly but significantly with early and late myocardial uptake and clearance rate (r = 0.277, P = .03; r = 0.421, P = .001; r = 0.382, P = .002; respectively) in patients with diabetes mellitus. CONCLUSION: Marked MIBG abnormalities are associated with left ventricular dysfunction in patients with diabetes mellitus. However, long-term follow-up of patients with diabetes mellitus who have marked MIBG abnormalities and normal LVEF will be required to determine whether these patients would demonstrate systolic dysfunction earlier than patients without an MIBG abnormality.

3-Iodobenzylguanidine↗

Preinfarction angina limits myocardial infarction size in nondiabetic patients treated with primary coronary angioplasty.

OBJECTIVE: To evaluate myocardial necrosis extent after myocardial infarction (MI) and reperfusion with primary coronary angioplasty in nondiabetic patients and the relationship with unstable preinfarction angina (PA). DESIGN: Prospective cohort study. SETTING: Studies suggest PA limits infarct size. This effect is questioned in patients treated with primary coronary angioplasty. PATIENTS: Seventy-eight, nondiabetic, consecutive MI patients. INTERVENTIONS: Primary coronary angioplasty and scintigraphic study to assess the myocardial infarct size. MAIN OUTCOME MEASURES: Scintigraphic myocardial infarct size. RESULTS: There were 32 patients with PA (PA +) and 46 without PA (PA -) in the 24-h period prior to MI onset. There were no significant differences in the baseline characteristics between the two groups. The scintigraphy indicated myocardial infarct size significantly smaller in PA + patients: mean, 18.0% (SD, 14.7) vs 27.0% (SD, 20.1) [p = 0.033]. This occurs even though Thrombolysis in Myocardial Infarction grade 3 flow achieved in both groups was similar (84.8% vs 84.4%, p = 1.000). We found a higher percentage of ST-segment resolution (>/= 70%) in PA + patients (65.6% vs 45.7%, p = 0.082) together with a lower incidence of left ventricular systolic dysfunction (3.2% vs 18.6%, p = 0.071). CONCLUSIONS: PA exerts a beneficial effect in nondiabetic patients with ST-segment elevation acute MI even when treated with primary PCI. The infarct size is limited, and left ventricular systolic function is preserved. The effects may be related to a better preservation of tissue reperfusion in patients with PA.

Angina Pectoris↗

Late complications and quality of life after atrial correction of transposition of the great arteries in 12 to 18 year follow-up.

BACKGROUND: Most adolescents and young adults born with transposition of the great arteries and survivors of Mustard operation are alive today and are leading ordinary lives. How far is the quality of their life influenced by residual findings? METHODS: We have analysed the oldest group of 177 children operated on with the Mustard procedure during 1979-1984 from our total experience of 609 corrections of transposition of the great arteries until 1996. In the long-term follow-up 12 to 18 years after Mustard operation the clinical investigation, 24 hours ECG Holter monitoring, 2D and colour flow Doppler echocardiography, radionuclide angiocardiography and exercise testing were performed. RESULTS: Basic sinus rhythm had 61% of 137 survivors, sinus node dysfunction had 51%. All but 4 patients needed no antiarrhythmic therapy. There were 10 sudden deaths. Severe tricuspid valve regurgitation developed in 15.9% of children, and decreased to 6% after intensive medical treatment. The right ventricular systolic dysfunction was found on radionuclide ventriculography in 8% of children after surgery. The left ventricular ejection fraction was subnormal in 10% and left ventricular diastolic function expressed by rapid filling fraction was subnormal in 80% of patients and may cause inability to increase cardiac output at exercise The obstruction of caval veins was found in 9%. There were neurological complications in 13.3% (10% already preoperatively) but severe brain damage was found in 4.4% only. CONCLUSIONS: Exercise tolerance with the maximum oxygen consumption over 30 ml/kg/min in 96% of investigated children suggests the good ability and full efficiency for recreation sports. Most survivors (84%) are reported to lead ordinary lives and function in NYHA class I.

Adolescent↗

Persistent preload defect in severe sepsis despite fluid loading: A longitudinal echocardiographic study in patients with septic shock.

STUDY OBJECTIVE: To investigate the rate of recovery from septic shock in patients with suspected left ventricular (LV) preload deficiency and LV systolic dysfunction. DESIGN: A monitoring period was defined by the need for inotropic/vasopressor support, and LV function was assessed daily during this period by bedside two-dimensional echocardiography (2D-ECHO). SETTING: University hospital ICU. PATIENTS: During a 5-year period, 90 patients with an episode of septic shock (60% with gram-positive bacteria as the causative agent) were consecutively enrolled in the study (mean age, 55 +/- 18 years). Standard volume resuscitation combined with inotropic/vasopressor support was used to maintain systolic arterial pressure > 90 mm Hg. All patients received mechanical ventilation because of associated respiratory failure. The average duration of hemodynamic support was 4.4 +/- 1.6 days. Thirty-four patients were weaned from hemodynamic support during the monitoring period and ultimately recovered (group I). Twenty-eight patients died from refractory circulatory failure during the monitoring period, and 28 died later from ARDS or multiple organ dysfunction syndrome, leading to a 62% overall mortality rate (group II). METHODS: Daily bedside LV volumes and ejection fraction (LVEF) were recorded using 2D-ECHO. Data obtained at the start (day 1 and day 2) and end of the monitoring period (day n) were compared. RESULTS: LV end-diastolic volume was within the normal range of our laboratory values in all patients, but was initially smaller in group II than in group I, and remained so despite fluid loading. LVEF was significantly depressed in all patients, resulting in severe reduction in LV stroke volume (LVSV), which was initially more marked in group I. In group I patients, LVEF significantly improved during the monitoring period, resulting in an increase in LVSV. CONCLUSION: 2D-ECHO changes during hemodynamic support in 90 septic patients confirmed defective LV preload with a propensity to worsen despite fluid loading in nonsurvivors (62% in the present study). Our results are also in agreement with previous studies reporting depressed LV systolic function at the initial phase of septic shock. Since LV dysfunction was more marked in patients who recovered, we suggest that the exact significance of this finding should be reevaluated.

Adult↗

Endothelin-1 has haemodynamic effects at pathophysiological concentrations in patients with left ventricular dysfunction.

OBJECTIVES: Plasma levels of immunoreactive endothelin-1 (ET-1) are raised in chronic heart failure. Whether plasma ET-1 contributes to the haemodynamic derangement found in chronic heart failure is not known. We investigated the effects of exogenous ET-1 on the pulmonary and systemic vasculature in patients with left ventricular systolic dysfunction (LVD), with or without overt heart failure. METHODS: ET-1 was infused at 1, 5 and 15 pmol/min into a distal pulmonary artery of ten patients with LVD to achieve plasma concentrations of ET-1 similar to those found in patients with heart failure and pulmonary hypertension. Haemodynamics were measured using a pulmonary thermodilution catheter and an arterial line. Intravascular Doppler and local pulmonary angiography were used to assess local pulmonary blood flow in the first four patients. RESULTS: Systemic haemodynamic changes occurred with ET-1 infusion: mean arterial pressure (100 +/- 3 [standard error of the mean]) to 107 +/- 3 mmHg; p < 0.01) and systemic vascular resistance (1699 +/- 118 to 2033 +/- 135 dynes s/cm5; p < 0.001) rose, while the cardiac index fell from 2.43 +/- 0.17 to 2.20 +/- 0.16 l/min/m2 (p < 0.002). Mean pulmonary artery pressure (21 +/- 2 mmHg) and pulmonary vascular resistance (151 +/- 14 to 147 +/- 14 dynes s/cm5) did not change however. CONCLUSIONS: Exogenous ET-1, when infused to achieve plasma concentrations similar to those in severe heart failure and pulmonary hypertension, causes systemic but not pulmonary vasoconstriction.

Aged↗

The effects of dyslipidemia on left ventricular systolic function in patients with stable angina pectoris.

Large-scale clinical trials have shown that long-term treatment with lipid-lowering therapy results in a significant reduction in the occurrence of heart failure among patients with coronary artery disease without previous evidence of congestive heart failure, suggesting dyslipidemia may have an adverse effect on left ventricular performance. To examine whether dyslipidemia has a detrimental effect on left ventricular systolic function and whether this effect is dependent on the corresponding severity of coronary atherosclerosis, 114 consecutive patients with stable angina and a positive exercise thallium-201 myocardial perfusion single-photon emission computed tomography were studied. All patients underwent measurement of serum lipid profiles, right-sided heart catheterization, left ventriculography, and selective coronary arteriography. Mean serum levels of total cholesterol and triglycerides were 4.5 and 1.4 mmol/l, respectively. In univariate analysis, a significant positive correlation between serum high-density lipoprotein (HDL) cholesterol and left ventricular ejection fraction (LVEF) (r = 0.49, P<0.0001) was found. Patients in the lower tertile of serum HDL cholesterol had a significantly lower mean LVEF than those in the upper tertile (55.9+/-15.2 vs. 72.8+/-6.8%, P<0.0001). Stepwise multiple linear regression analysis revealed that LVEF significantly correlated with HDL cholesterol (P<0.0001), the Gensini score (P = 0.008), and diabetes mellitus (P = 0.08) (r = 0.55, P<0.0001). In subgroup analysis of patients with angiographically normal coronary arteries, serum HDL cholesterol was still significantly associated with LVEF. The present study demonstrated an independent association between low HDL cholesterol and subclinical left ventricular systolic dysfunction in Chinese patients with stable angina whose serum levels of total cholesterol and triglycerides were relatively low. Moreover, this correlation remained significant even in patients with normal coronary angiograms, suggesting HDL cholesterol might influence left ventricular systolic performance through extra-atherosclerotic mechanisms.

Aged↗

Coronary microvascular dysfunction and ischemia in hypertrophic cardiomyopathy. Mechanisms and clinical consequences.

Symptoms and signs of myocardial ischemia are often found in patients with hypertrophic cardiomyopathy (HCM) despite angiographically normal coronary arteries. Myocardial ischemia is deemed responsible for some of the lethal complications of HCM including ventricular arrhythmias, sudden death, progressive left ventricular remodeling, and systolic dysfunction. In the past decade, a number of studies using positron emission tomography have demonstrated severe impairment of the vasodilator response to dipyridamole in the majority of HCM patients, not only in the hypertrophied septum but also in the non-hypertrophied left ventricular free wall. In the absence of coronary stenoses, this finding is indicative of diffuse microvascular dysfunction, in line with the autoptic evidence of widespread abnormalities of the intramural coronary arterioles. In turn, microvascular dysfunction represents a very likely substrate for recurrent ischemia. This may account for the fact that microvascular dysfunction has recently been shown to represent an early and powerful predictor of an unfavorable outcome in HCM. The aim of this article is to provide a concise overview of the available evidence of microvascular dysfunction and ischemia in HCM, and to speculate on the potential implications for management.

Cardiomyopathy, Hypertrophic↗

Age-related differences in the response to myocardial ischemic stress.

Clinical experience indicates that the risk of reparative cardiac operations is increased in the neonatal period relative to that in older infants and children. Age-related differences in the susceptibility to myocardial ischemic dysfunction were evaluated by comparison of left ventricular function and metabolism in neonatal (mean age = 7 days) and weanling (mean age = 96 days) piglets. Six animals in each group supported on cardiopulmonary bypass were subjected to (1) 120 minutes of hypothermic crystalloid cardioplegic arrest (CP-120) and (2) 15 minutes of normothermic ischemic arrest (NA-15) after a 60 minute interval of reperfusion. Left ventricular systolic and diastolic function was measured after each intervention via endocardially implanted ultrasonic dimension crystals in a septolateral minor-axis position. In both groups, systolic dysfunction was evidenced by an increase in the dimension-axis intercept (p = 0.001), but not the slope of the end-systolic pressure-dimension relation. Left ventricular end-diastolic stiffness, expressed as left ventricular end-diastolic pressure versus Lagrangian strain, increased to a similar degree in both groups (p = 0.001). Adenosine triphosphate levels declined significantly (p = 0.001) in both groups in response to the ischemic interventions with no evident intergroup differences. Lactate levels increased significantly during the course of the experiment (p = 0.04); however, the increases were greater (p = 0.009) at all intervals in the neonatal group. This study demonstrates age-related metabolic differences in response to ischemia consistent with a greater dependence on glycolysis in neonatal myocardia. However, the fact that discriminating age-related differences in left ventricular function were not evident suggests that factors other than young age per se account for the increased surgical mortality in the neonatal period.

Adenosine Triphosphate↗

Accuracy of B-type natriuretic peptide levels in the diagnosis of left ventricular dysfunction and heart failure: a systematic review.

OBJECTIVES: To evaluate the accuracy of B-type natriuretic peptide levels (BNP) in the diagnosis of heart failure and left ventricular dysfunction. DATA SOURCES: Electronic search in Medline, Embase, Cochrane Library and Medion database, and hand search of reference lists. REVIEW METHODS: We have included published studies on the accuracy of BNP which had both sufficient information to construct the 2x2 diagnostic cross table and an appropriate spectrum of patients. RESULTS: Fifty five studies (16,730 patients) were analyzed. The main determinants of diagnostic accuracy were the reference standard analyzed (clinical heart failure versus left ventricular dysfunction), and the methodological quality of the study. BNP levels were highly accurate for the diagnosis of clinical heart failure (diagnostic OR=41; 95% CI 23-74). The negative likelihood ratios were homogeneous, and useful for excluding the existence of heart failure (pooled negative likelihood ratio=0.11; 95% CI 0.08-0.16). The studies focused on the identification of left ventricular dysfunction were heterogeneous, with indications of publication bias, and showed less overall diagnostic accuracy than studies focused on heart failure. CONCLUSIONS: BNP levels are useful for ruling out heart failure. The accuracy of BNP for identifying patients with systolic dysfunction is more limited.

Cardiac Output, Low↗

Transthoracic echocardiography to identify or exclude cardiac cause of shock.

BACKGROUND: Transesophageal echocardiography (TEE) is often still considered the echocardiographic test of choice in the general ICU patient population to establish the presence or absence of cardiac cause of shock, and is often requested and performed as the initial and only echocardiographic test. This premise is based on older studies in which transthoracic echocardiography (TTE) commonly offered inadequate images in ICU patients. STUDY OBJECTIVES: We hypothesized that current TTE imaging alone is adequate to identify or exclude cardiac cause of shock in the great majority of cases. METHODS: One hundred consecutive shock cases in which an echocardiogram was requested were prospectively analyzed by two blinded echocardiographers for image adequacy, and the absence or presence of cardiac cause of shock (defined as one or more of the following: severe left ventricular (LV) or right ventricular systolic dysfunction, tamponade, severe left-sided valve disease, or a postinfarction mechanical complication), and compared to a clinical standard of presence/absence of cardiac cause of shock as determined by autopsy, surgery, or objective testing. Shock was defined as systolic BP < 100 mm Hg or fall in BP >/= 25%, and inotrope use or evidence of low output or venous congestion. Cardiac output was determined by the LV outflow tract (LVOT) Doppler method. RESULTS: Sixty-three percent of cases had a cardiac cause of shock. TTE image quality was adequate in 99% cases. Among the 99% of cases in which the imaging was adequate, the sensitivity of TTE for cardiac cause of shock was 100%, the specificity was 95%, the positive predictive value was 97%, and the negative predictive value was 100%. There were relative contraindications to TEE in 15% of cases. Stroke volume index (15 +/- 6 mL/m(2) vs 31 +/- 7 mL/m(2) [mean +/- 1 SD]; p < 0.001) and cardiac index (1.6 +/- 0.5 mL/min/m(2) vs 2.9 +/- 0.9 mL/min/m(2); p < 0.001) were significantly less in the group with a cardiac cause of shock than in the group with a noncardiac cause of shock. CONCLUSIONS: In the general critical care population, current TTE imaging identifies the great majority of cardiac causes of shock. TTE should be considered not only the initial, but also the principal echocardiographic test in the critical care environment.

Aged↗

Evolving rationale for angiotensin-converting enzyme inhibition in chronic heart failure.

The rationale behind the use of angiotensin-converting enzyme (ACE) inhibitors has evolved considerably since their approval for the treatment of hypertension. The initial rationale behind their use for the treatment of chronic heart failure was to duplicate with one agent the hemodynamic effects produced by the hydralazine-isosorbide dinitrate combination, i.e., increasing cardiac output while reducing ventricular filling pressures. The observation that the acute hemodynamic effects of ACE inhibitors did not predict long-term clinical benefits led to the search for mechanisms other than hemodynamic improvement. Attenuation or even reversal of left ventricular dilatation after myocardial infarction, which was first reported with ACE inhibition in an experimental model of myocardial infarction and subsequently in patients with recent myocardial infarction, provided a new rationale for the use of these inhibitors for chronic heart failure. However, this apparent prevention of left ventricular dilatation by ACE inhibitors is less apparent in patients with congestive heart failure due to left ventricular systolic dysfunction (decreased ejection fraction) than in patients with recent myocardial infarction. Furthermore, the unexpected finding that long-term ACE inhibition decreases the incidence of recurrent myocardial infarction in patients with coronary artery disease and an already reduced systolic function, suggested the hypothesis that vascular protection may provide most of the clinical benefits of ACE inhibitors. This hypothesis was successfully tested by demonstrating a lower incidence of cardiovascular events in high-risk vascular patients randomized to long-term ACE inhibition with ramipril. Accordingly, the current rationale behind the use of ACE inhibitors in patients with chronic heart failure is largely that of vascular protection.

Angiotensin-Converting Enzyme Inhibitors↗