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At least 343 records · Page 19Linked to original sources
PubMed2004

The efficacy of azimilide in the treatment of atrial fibrillation in the presence of left ventricular systolic dysfunction: results from the Azimilide Postinfarct Survival Evaluation (ALIVE) trial.

OBJECTIVES: The purpose of this study was to assess the effect of oral azimilide dihydrochloride (AZ) 100 mg versus placebo on the onset, termination, and prevalence of atrial fibrillation (AF) in a subpopulation of patients in the Azimilide Postinfarct Survival Evaluation (ALIVE) trial. BACKGROUND: Previous clinical trials have demonstrated the antiarrhythmic effects of AZ in patients with AF. Azimilide was investigated for its effects on mortality in patients with depressed left ventricular (LV) function after recent myocardial infarction (MI) and in a subpopulation of patients with AF. METHODS: A total of 3,381 post-MI patients with depressed LV function were enrolled in this randomized, placebo-controlled, double-blind study of AZ 100 mg on all-cause mortality. A total of 93 patients had AF on the baseline 12-lead electrocardiogram (ECG). An additional 27 patients developed AF after initially being in sinus rhythm at randomization. These patients were identified through 12-lead ECGs obtained during routine visits at week 2, months 1, 4, 8, and 12. RESULTS: Patients with AF at baseline had a higher mortality than those without AF (p = 0.0006). Among AF patients, there was no difference in mortality between AZ patients and placebo patients (p = 0.82). Fewer AZ patients developed AF than placebo patients (p = 0.04). More AZ patients than placebo patients converted to sinus rhythm, but this difference did not achieve statistical significance (p = 0.076). Over one-year follow-up, more AZ patients were in sinus rhythm than placebo patients (p = 0.04). CONCLUSIONS: Azimilide was safe and effective AF therapy in patients with depressed LV function after an MI.

Adrenergic beta-Antagonists↗
PubMed2000

Left ventricular thrombus and subsequent thromboembolism in patients with severe systolic dysfunction.

STUDY OBJECTIVES: To determine the frequency of left ventricular (LV) thrombi by echocardiography and to define the predictors of LV thrombus and subsequent thromboembolism. DESIGN: Retrospective case-control design. SETTING: Single tertiary care center. PATIENTS: Twenty-eight patients with LV thrombus in a consecutive series of 144 patients with severe LV dysfunction and follow-up period for a mean of 27.6 months. MEASUREMENTS AND RESULTS: Thirty-five clinical and echocardiographic variables were evaluated. The mean age of patients with (n = 28) vs patients without (n = 116) LV thrombus was 50.3 +/- 11.0 years vs 54.2 +/- 11.1 years (p = 0.09), with 22 patients (78.6%) and 78 patients (67.2%) being male (p = 0.24), respectively. The mean ejection fraction (EF) for those with vs those without LV thrombus was 17.5 +/- 5.5 vs 20.0 +/- 6.9 (p = 0. 08), with 16 patients (57.1%) and 42 patients (36.2%) having an EF < 20% (p = 0.04), respectively. The groups were similar with respect to other baseline characteristics, comorbid illnesses, and drug therapies other than anticoagulants. All 28 patients with LV thrombus (100%) and 54 of those without LV thrombus (46.6%) were treated with warfarin. Ischemic etiology of the cardiomyopathy (odds ratio, 4.78; 95% confidence interval, 1.51 to 15.11; p = 0.008) and increased LV internal diastolic dimension (LVIDD; odds ratio, 1.10; 95% confidence interval, 1.03 to 1.18; p = 0.004) were found to be independent predictors of thrombus formation. Peripheral embolism occurred in 5 patients (17.9%) vs 13 patients (11.2%) of those with and without LV thrombi, respectively (p = 0.35). Ischemic etiology of the cardiomyopathy (odds ratio, 3.79; 95% confidence interval, 1. 13 to 12.64; p = 0.03) and EF (odds ratio, 0.91; 95% confidence interval, 0.82 to 1.00; p = 0.04) were found to be independent predictors of systemic embolization. The patients with an embolic event suffered a significantly higher mortality (7 of 18 patients; 38.9%) during the follow-up period when compared to those without an embolic event (13 of 126 patients; 10.3%; p < 0.0001). CONCLUSIONS: We conclude that ischemic cardiomyopathy and dilated LV chamber sizes (LVIDD > 60 mm) are independently associated with LV thrombi. A peripheral embolic event is related to poor long-term survival in this patient group.

Adult↗
PubMed2002

Antithrombotic therapy is associated with better survival in patients with severe heart failure and left ventricular systolic dysfunction (EPICAL study).

BACKGROUND: In patients with congestive heart failure (CHF), clinical trials have demonstrated the benefit of a number of drugs on morbidity and mortality. Nevertheless so far, there is no published controlled study of long-term antithrombotic therapy in patients with CHF. The aim of this work was to identify the relationship between cardiovascular drug use, especially antithrombotic therapy, and survival of CHF patients in current clinical practice, using an observational, population-based database. METHODS: The EPICAL study (Epidémiologie de l'Insuffisance Cardiaque Avancée en Lorraine) has identified prospectively all patients with severe CHF in the community of Lorraine. Inclusion criteria were age 20-80 years in 1994, at least one hospitalisation for cardiac decompensation, NYHA III/IV HF, ventricular ejection fraction < or =30% or cardiothoracic index > or =60% and arterial hypotension or peripheral and/or pulmonary oedema. A total of 417 consecutive patients surviving at hospital discharge were included in the database. The average follow-up period was 5 years. Univariate Cox models were used to test the relationship of baseline biological and clinical factors to survival. Cardiovascular drug prescriptions were tested in a multivariate Cox model adjusted by other known predictive factors. RESULTS: Duration of disease >1 year, renal failure, serum sodium > or =138 mmol/l, old age, serious comorbidity, previous decompensation, high doses of furosemide and vasodilators use were independently associated with poor prognosis at 1 and 5 years. Oral anticoagulants, aspirin, lipid lowering drugs and beta-blockers use were associated with better survival. There was no interaction between aspirin and angiotensin converting enzyme inhibitor use on survival. CONCLUSION: Antithrombotic therapy was associated with a better long-term survival in our study population of severe CHF. These results together with other previously published circumstantial evidence urge for a prospective, controlled and randomised trial specifically designed to evaluate optimal oral anticoagulants and aspirin in patients with congestive heart failure.

Adrenergic beta-Antagonists↗
PubMed2006

Usefulness of ventricular longitudinal contractility assessed by Doppler tissue imaging in the prediction of reverse remodeling in patients with severe left ventricular systolic dysfunction.

OBJECTIVE: We sought to test if assessment of ventricular longitudinal contractility (LC) by Doppler tissue imaging (DTI) can predict reverse remodeling (RR) of left ventricular (LV) dysfunction resulting from medical treatment. METHODS: DTI was performed in 35 patients with nonischemic LV dysfunction (ejection fraction 26 +/- 7%) and LC was assessed at the 4 different basal segments of the LV walls (septal, lateral, inferior, and anterior) using myocardial velocity curves and strain measurements; the peak systolic or delayed longitudinal contraction velocity of LV walls only with concomitant negative strain were measured and added to represent LC of each patient (LC by DTI). Successful RR was defined as a reduction of LV end-systolic volume of greater than 15%. RESULTS: RR was observed in 13 patients (37%, group A). Initial LV ejection fraction was similar in patients who did and did not achieve RR (group B). Compared with group B, group A showed shorter QRS interval (110 +/- 36 vs 136 +/- 28 milliseconds, P = .022), shorter symptom duration (2.3 +/- 3.5 vs 4.2 +/- 3.4 years, P = .047), lower prevalence of left bundle branch block (23% vs 59%, P = .039), and higher value of LC by DTI (9.6 +/- 3.5 vs 6.3 +/- 3.6 cm/s, P = .011). Multivariate analysis revealed that symptom duration less than 2 years (odds ratio = 8.0, 95% confidence interval = 1.3-47.2, P = .022) and LC by DTI (odds ratio = 1.3, 95% confidence interval = 1.0-1.7, P = .019) were independent predictors of RR. CONCLUSIONS: DTI provides a new index of LC, which is useful for predicting RR in patients with severe LV dysfunction.

Cardiomyopathy, Dilated↗
PubMed1982

The role of right ventricular systolic dysfunction and elevated intrapericardial pressure in the genesis of low output in experimental right ventricular infarction.

To elucidate the pathophysiology of severe right ventricular infarction (RVI), isolated RVI was produced in 15 dogs with the pericardium intact or open. After RVI in dogs with the pericardium intact, RV systolic pressure decreased by 27%, aortic pressure by 29% and cardiac output by 34%. RV transmural pressure, RV end-diastolic size and intrapericardial pressure increased, left ventricular transmural pressure and end-diastolic size decreased and the diastolic pressures equalized. Pericardiotomy after RVI resulted in increased ventricular transmural pressures and diastolic size, improved cardiac output and resolution of equalized diastolic pressures. RVI in dogs with the pericardium open resulted in similar changes, but of lesser magnitude and without equalization of diastolic pressures. These results indicate that reduced left ventricular preload due to impaired RV systolic function contributes to low cardiac output in RVI. Elevated intra-pericardial pressure further reduced left ventricular preload and produces equal diastolic pressures.

Animals↗
PubMed1993

Left ventricular systolic dysfunction precipitated by verapamil in cardiac amyloidosis.

Cardiac amyloidosis produces a restrictive cardiomyopathy with impaired diastolic function. We report a case in which low-dose verapamil resulted in marked worsening of congestive heart failure, as a result of a profound negative inotropic effect. Withdrawal of verapamil therapy demonstrated a return of systolic function to normal with improvement in heart failure. We postulate that patients with cardiac amyloidosis may be exceptionally sensitive to the negative inotropic effects of calcium-channel blockers either because of abnormal binding to amyloid fibrils or because their usual vasodilator effects are blunted.

Amyloidosis↗
PubMed2000

Profile of plasma N-terminal proBNP following acute myocardial infarction; correlation with left ventricular systolic dysfunction.

AIMS: The aims of this study were to describe the temporal pattern of plasma N-terminal pro-brain natriuretic peptide, to examine the optimum time of sampling and to compare plasma N-terminal pro-brain natriuretic peptide to clinical criteria in terms of identification of impaired left ventricular systolic function following acute myocardial infarction. METHODS AND RESULTS: Measurements of N-terminal pro-brain natriuretic peptide were made in 60 patients at 14-48 h, 49-72 h, 73-120 h, 121-192 h following myocardial infarction and at 6 weeks in survivors. Left ventricular wall motion index was assessed during hospitalization (WMI-1) and at 6 weeks (WMI-2). N-terminal pro-brain natriuretic peptide levels were elevated at all time points, to a greater extent in anterior compared to inferior infarction (P < 0.05). A biphasic profile of plasma concentration was observed in anterior infarction with peaks at 14-48 h and 121-192 h. This was sustained at 6 weeks. N-terminal pro- brain natriuretic peptide at 73-120 h was the best independent predictor of WMI-1 (P < 0.005). N-terminal pro-brain natriuretic peptide was higher at all times in patients who received ACE inhibitor therapy compared to those who did not (P < 0.005). N-terminal pro-brain natriuretic peptide at 73-120 h (R(2) = 17.7%, P = 0.005) and previous myocardial infarction (R(2) = 5.3%, P < 0.05) were independent predictors of poor outcome (WMI-2 < or = 1.2 or death by 6 weeks). CONCLUSIONS: A biphasic pattern of plasma N-terminal pro-brain natriuretic peptide is seen after anterior myocardial infarction. Plasma level is strongly correlated to wall motion index soon after and remote from acute myocardial infarction. Plasma N-terminal pro-brain natriuretic peptide measured later in hospitalization better predicts poor outcome following myocardial infarction than when it is measured in the immediate post infarction period.

Adult↗
PubMed2004

Serum cardiac troponin T in patients hospitalized with heart failure is associated with left ventricular hypertrophy and systolic dysfunction.

BACKGROUND: Cardiac troponin T (cTnT) is a highly sensitive and specific marker of acute myocardial infarction. Serum cTnT is also slightly elevated in patients with severe heart failure and is associated with left ventricular hypertrophy (LVH) in patients treated with haemodialysis. In this study serum cTnT concentrations and echocardiographic findings were investigated in heart failure patients without acute coronary syndrome. cTnT was also compared with other cardiac markers and plasma levels of brain natriuretic peptide (BNP). METHODS: Twenty-six patients hospitalized with heart failure were included in the study. Echocardiographic measurements and blood sampling were carried out 12-36 h after admission. Serum cTnT (3rd generation assay), cardiac troponin I (cTnI), creatine kinase MB (CKMB) and CK were measured. Plasma BNP was analysed using the Shionoria assay. LVH was defined as left ventricular mass index (LVMI) > 125 g/m for males and > 110 g/m for females. Left ventricular systolic function was estimated from the mitral annulus motion (AV-mean LV). RESULTS: Median cTnT was 0.012 (< 0.010-0.032) microg/L. Sixty-two percent of the patients (16 of 26) had elevated serum cTnT >or= 0.010 micro/L. cTnT was positively correlated with CKMB (rho = 0.40, p = 0.04) and BNP (rho = 0.43, p = 0.03), but not with cTnI and CK. A negative correlation was found between cTnT and AV-mean LV (rho = -0.58, p = 0.007), and there was a positive correlation between cTnT and LVMI (rho = 0.44, p = 0.03). No other analyte was correlated to LVMI. CONCLUSIONS: Serum cTnT but not cTnI was associated with left ventricular dysfunction and LVH in patients hospitalized with heart failure. This explains why cTnT tends to be slightly elevated in patients with heart failure without symptoms of acute myocardial ischaemia.

Aged↗
PubMed2005

Left ventricular systolic dysfunction after transcatheter closure of a large patent ductus arteriosus.

A 12-year-old boy reported in outpatient department with history of shortness of breath and dyspnoea on moderate exertion. Physical examination was significant for bounding pulses and for a continuous murmur III/VI, best heard at the left upper sternal border. Echocardiography confirmed a large patent arterial duct with shortening fraction of 33%. He underwent successful transcatheter closure of the patent arterial, using Amplatzer duct occluder 12/10. Few hours later echocardiography revealed an unexpected, yet important depression of left ventricular systolic function with shortening fraction decreasing to 24% and then two weeks later decreasing further to 20%. At a follow-up after four months, he had improved clinically but left ventricular dysfunction still persisted with shortening fraction of 24%.

Cardiac Catheterization↗
PubMed1995

Residual exertional ischemia and unfavorable left ventricular remodeling in patients with systolic dysfunction after anterior myocardial infarction.

OBJECTIVES: This study investigated whether exercise-induced myocardial ischemia influences left ventricular remodeling after anterior myocardial infarction. BACKGROUND: The effects of acute and recurrent ischemia on ventricular function are well established. However, to our knowledge the role of exertional ischemia in the remodeling response after infarction has not been investigated. METHODS: Ninety-one patients with a first anterior Q wave myocardial infarction were studied at 5 weeks by rest echocardiography and exercise scintigraphy. The echocardiographic examination was repeated 6 months later. On the basis of the presence and extent of reversible perfusion defects on exercise scintigraphy, patients were assigned to groups with no exertional ischemia (group 1, n = 20 [22%], mild to moderate ischemia (group 2, n = 45 [49%]) and severe exertional ischemia (group 3, n = 26 [29%]). RESULTS: Initial left ventricular volumes were similar, and no differences were found among the three groups in the remodeling response over the 6-month period of the study. However, patients in groups 2 and 3 with an ejection fraction < or = 40% showed significant (p < 0.01) ventricular enlargement over time, which was similar between the two groups (end-diastolic volume [mean +/- SD] from 74 +/- 13 to 80 +/- 17 ml/m2 in group 2 and from 72 +/- 11 to 81 +/- 19 ml/m2 in group 3; regional dilation from 42 +/- 16% to 52 +/- 22% in group 2 and from 38 +/- 18% to 46 +/- 27% in group 3). In contrast, ventricular dimensions did not change in group 1 patients with an ejection fraction < or = 40% as well as in patients in all three groups with an ejection fraction > 40%. CONCLUSIONS: Exercise-induced myocardial ischemia may contribute to progressive ventricular enlargement in patients with poor left ventricular function after a large anterior myocardial infarction.

Analysis of Variance↗
PubMed2005

Mortality and morbidity remain high despite captopril and/or Valsartan therapy in elderly patients with left ventricular systolic dysfunction, heart failure, or both after acute myocardial infarction: results from the Valsartan in Acute Myocardial Infarction Trial (VALIANT).

BACKGROUND: The elderly constitute an increasing proportion of acute myocardial infarction patients and have disproportionately high mortality and morbidity. Those with heart failure or impaired left ventricular left ventricular function after acute myocardial infarction have high complication and mortality rates. Little is known about outcomes with contemporary therapies in these patients. METHODS AND RESULTS: The Valsartan in Acute Myocardial Infarction Trial (VALIANT) randomized 14,703 patients with heart failure and/or left ventricular ejection fraction <40% to receive captopril, valsartan, or both. Mortality and a composite end point, including cardiovascular mortality, readmission for heart failure, reinfarction, stroke, and resuscitated cardiac arrest, were compared for the age groups of <65 (n=6988), 65 to 74 (n=4555), 75 to 84 (n=2777), and > or =85 (n=383) years. With increasing age, 3-year mortality almost quadrupled (13.4%, 26.3%, 36.0%, and 52.1%, respectively), composite end-point events more than doubled (25.2%, 41.0%, 52.3%, and 66.8%), and hospital admissions for heart failure almost tripled (12.0%, 23.1%, 31.3%, and 35.4%). Outcomes did not differ between the 3 study treatments in any age group. Adverse events associated with captopril and valsartan were more common in the elderly and in patients receiving combination therapy. With increasing age, use of aspirin, beta-blockers, and statins declined, and use of digoxin, calcium-channel blockers, and non-potassium-sparing diuretics increased. On 3-year multivariable analysis, each 10-year age increase was associated with a hazard ratio of 1.49 (95% CI, 1.426 to 1.557; P<0.0001) for mortality and an odds ratio of 1.38 (95% CI, 1.31 to 1.46; P<0.0001) for readmission with heart failure. CONCLUSIONS: Outcomes remained poor in elderly patients with heart failure and/or impaired left ventricular systolic function after acute myocardial infarction, although most received beta-blockers and all received an ACE inhibitor and/or an angiotensin receptor blocker. Better therapies and increased use of aspirin, beta-blockers, and statins are needed in this important and increasing patient group.

Age Factors↗
PubMed2002

Plasma cardiotrophin-1 following acute myocardial infarction: relationship with left ventricular systolic dysfunction.

The glycoprotein 130 (gp 130) signalling pathway is important in the development of heart failure. Cardiotrophin-1 (CT-1), a cytokine acting via the gp 130 pathway, is involved in the process of ventricular remodelling following acute myocardial infarction (AMI) in animals. The aims of the present study were to examine the profile of plasma CT-1 following AMI in humans, and its relationship with echocardiographic parameters of left ventricular (LV) systolic function. Serial measurements of plasma CT-1 levels were made in 60 patients at 14-48 h, 49-72 h, 73-120 h and 121-192 h following AMI and at a later clinic visit. LV function was assessed using a LV wall motion index (WMI) score on admission (WMI-1) and at the clinic visit (WMI-2). Compared with values in control subjects (29.5+/-3.6 fmol/ml), the plasma CT-1 concentration was elevated in AMI patients at 14-48 h (108.1+/-15.1 fmol/ml), 49-72 h (105.2+/-19.7 fmol/ml), 73-120 h (91.2+/-14.9 fmol/ml) and 121-192 h (118.8+/-22.6 fmol/ml), and at the clinic visit (174.9+/-30.9 fmol/ml) (P<0.0001). Levels were higher following anterior compared with inferior AMI. For patients with anterior AMI, CT-1 levels were higher at the clinic visit than at earlier times. WMI-1 correlated with CT-1 at all times prior to hospital discharge (P<0.05). On best subsets analysis, the strongest correlate with WMI-1 was CT-1 level at 49-72 h (R(2)=20%, P<0.05). In conclusion, plasma levels of CT-1 are elevated soon after AMI in humans and rise further in the subsequent weeks in patients after anterior infarction. CT-1 measured soon after AMI is indicative of LV dysfunction, and this cytokine may have a role in the development of ventricular remodelling and heart failure after AMI.

Adult↗
PubMed1998

Preoperative left ventricular systolic dysfunction correlates with the adverse postoperative consequences of annular-papillary disconnection in the course of mitral valve replacement for stenosis.

BACKGROUND AND AIMS OF THE STUDY: Preservation of chordae tendineae helps maintain ventricular performance in patients having surgery for mitral regurgitation. The importance of chordal integrity in patients with rheumatic mitral stenosis is unknown. The purpose of this study was to determine the influence of chordal preservation on left ventricular function following relief of rheumatic mitral stenosis. METHODS: A total of 142 patients with mitral stenosis had balloon valvulotomy (group 1, n = 63), surgical commissurotomy (group 2, n = 33) or mitral valve replacement (group 3, n = 46). Chordae were resected in all group 3 patients. Left ventricular dimension in end-diastole (LVEDD), end-systole (LVESD) and fractional shortening (FS) were measured at baseline and at a mean interval of 11 +/- months post intervention. RESULTS: At one year, FS increased in groups 1 and 2, but decreased in group 3 (+11.5%, +9%, -6.1%, p < 0.005 for group 3 versus groups 1 and 2). a borderline significant increase LVEDD was seen in group 1 compared with groups 2 and 3 (11%, 5%, 4% respectively, p = 0.05). Differences in FS at follow up were due mainly to diametrically opposite changes in LVESD in the subgroup of patients with baseline left ventricular dysfunction (-1.9%, 0%, +9.8%, p < 0.005 for group 3 versus groups 1 and 2). CONCLUSIONS: Deterioration of left ventricular function only in patients having mitral valve replacement indicates chordal resection as a putative mechanism. The result of this study suggest that chordal preservation is particularly important in patients with mitral stenosis who have depressed preoperative left ventricular systolic function.

Adult↗
PubMed1992

[A case of hypereosinophilic syndrome exhibiting left ventricular systolic dysfunction].

A 16-year-old woman suffering from bronchial asthma since 2 years previously was admitted to the hospital because of high grade fever, dyspnea, skin eruption and arthralgia. Laboratory data revealed pronounced eosinophilia with elevated immunoglobulin E value. A chest X-ray film showed cardiomegaly with pulmonary congestion. Left ventriculograms showed diffusely reduced motion of the left ventricle (LV). Various clinical symptoms and laboratory data were resolved shortly after the administration of corticosteroids, but the LV dysfunction persisted for at least three months. Left ventriculograms 2 years later disclosed a marked improvement of the LV wall motion. In both the acute and the chronic phase, endomyocardial biopsy of both ventricles revealed non-specific histological findings comprising disarrangement of myocytes and interstitial fibrosis, suggesting post-myocarditis. This case was characterized by LV dysfunction possibly due to eosinophilic myocarditis associated with hypereosinophilic syndrome, and by its functional improvement with long-term corticosteroid therapy.

Adolescent↗
PubMed2005

Neonatal glucocorticosteroid treatment causes systolic dysfunction and compensatory dilation in early life: studies in 4-week-old prepubertal rats.

Glucocorticosteroid treatment is widely used to prevent chronic lung disease in premature infants. Recent studies in adult rats, treated with dexamethasone in the neonatal period, report negative long-term effects on the heart and severely reduced life expectancy. We treated neonatal rats with dexamethasone and studied cardiac function after 4 wk (prepubertal age) to investigate whether the late effects as previously described are preceded by detectable alterations in cardiac function at a younger age. Male rat pups (n = 12) were injected intraperitoneally with dexamethasone on d 1, 2, and 3 (0.5, 0.3, and 0.1 mug/g) of life. Control pups (n = 10) received saline. At 4 wk the animals were anesthetized, and a pressure-conductance catheter was introduced into the left ventricle to measure pressure-volume loops. Cardiac function was measured and pressure-volume relations were determined to quantify intrinsic systolic and diastolic function. Subsequently, hearts were excised for histologic examination. Compared with saline-treated animals, dexamethasone-treated rats had a reduced ventricular weight (270 +/- 40 versus 371 +/- 23 mg, p < 0.001) and reduced systolic function (end-systolic elastance: 1.24 +/- 0.43 versus 2.50 +/- 1.39 mm Hg/muL, p = 0.028). Cardiac output was maintained and end-diastolic volume was increased (84 +/- 23 versus 59 +/- 19 microL, p = 0.012) indicating a state of compensatory dilatation. Heart rate, diastolic function, and systemic vascular resistance were unchanged. Neonatal dexamethasone treatment causes cardiac alterations that can be detected in the prepubertal period and that may precede severe cardiac dysfunction later in life. If our findings are confirmed in humans, this may have consequences for a large patient population and cardiac screening at young age may be indicated to enable secondary prevention.

Animals↗