Form Of Left Ventricular Dysfunction Research Articles

Monitoring for Chemotherapy-Related Cardiotoxicity in the Form of Left Ventricular Systolic Dysfunction: A Review of Current Recommendations.

Cardiotoxicity is a well-established complication of multiple cancer therapeutics, and the one of the most prominent effects that limits the use of these agents is in the form of left ventricular dysfunction, otherwise known as chemotherapy-induced cardiomyopathy (CIMP). Because CIMP can worsen patient outcomes and interfere with a patient's life-saving cancer treatments, it is important to implement a monitoring strategy for patients undergoing potentially cardiotoxic treatments. Efforts have been made by multiple societies to provide recommendations for screening and monitoring for CIMP in at-risk patients, with slight variations between guideline documents and expert consensuses. Most of the recommendations for monitoring for CIMP are specific to anthracyclines and the human epidermal growth factor receptor 2-antagonist trastuzumab, with very limited guidance for other cardiotoxic agents such as Tyr kinase inhibitors and proteasome inhibitors, which we cover in this article. Echocardiography remains the mainstay for imaging surveillance because of its safety profile and widespread availability, but the accuracy of cardiac magnetic resonance imaging (CMR) makes it an important modality when there are discrepancies in left ventricular ejection fraction assessment. Subclinical cardiotoxicity may be detected using laboratory biomarkers such as cardiac troponin and brain natriuretic peptide as well as myocardial deformation (strain) imaging by echocardiography or CMR. Specific recommendations for timing and frequency of laboratory biomarker assessment remain up for debate, but myocardial deformation imaging should be performed with every echocardiogram or CMR assessment. Future studies are needed to evaluate the efficacy of established surveillance recommendations and to develop specific recommendations for novel cancer therapeutics.

Could CMR Tissue-Tracking and Parametric Mapping Distinguish Between Takotsubo Syndrome and Acute Myocarditis? A Pilot Study

Takotsubo syndrome (TS) is a transient and often misdiagnosed form of left ventricular dysfunction. Acute myocarditis (AM) is usually included in TS differential diagnosis. The aim of this study is to assess the role of cardiac magnetic resonance imaging coupled with tissue-tracking technique (CMR-TT) and parametric mappings analysis in discriminating between TS and AM. We retrospectively enrolled three groups: patients with TS (n = 12), patients with AM (n = 14), and 10 healthy controls. All the patients had a comprehensive CMR examination, including the assessment of global and segmental longitudinal strain, circumferential strain, radial strain (RS), and parametric mapping. The analysis of variance was used to compare the different groups. In TS patients, basal RS, global T1 mapping, global T2 mapping, mid T2 mapping, apical T1 and T2 mapping were statistically significantly different compared with the other groups. MANCOVA analysis confirmed that the association between myocardial strain data and parametric mapping was independent on age and sex. Apical T1 and T2 mapping proved to have a good performance in differentiating TS from AM (area under the curves of 0.908 and 0.879, respectively). Basal RS and apical tissue mapping analysis are the most advanced CMR-derived parameters in making a differential diagnosis between TS and AM.

EFFECTS OF TYPE 2 DIABETES MELLITUS ON CLINICAL AND LABORATORY STATUS OF WOMEN WITH ARTERIAL HYPERTENSION, OBESITY, AND LEFT VENTRICULAR DIASTOLIC DYSFUNCTION

Patients with type 2 diabetes mellitus (DM) may develop cardiomyopathy independently of such risk factors as arterial hypertension and coronary heart disease. Myocardial dysfunction in diabetes mellitus may vary from subclinical forms of left ventricular dysfunction to heart failure. It was suggested that diastolic left ventricular dysfunction is one of the earliest signs of myocardial injury in diabetes mellitus and plays a key role in the formation of diabetic cardiomyopathy. The aim of our study was to evaluate the effect of diabetes on the clinical and laboratory status of women with hypertension, obesity, and left ventricular diastolic dysfunction (LVDD). Materials and methods. We examined 80 patients aged 40 to 60 years with stage 2, grade II and grade III hypertension, class I–III obesity, grade 1 LVDD and preserved ejection fraction. Depending on the presence or absence of diabetes, the cohort of patients was divided into two groups: patients with diabetes were assigned to group 1 and non-diabetes patients ­­– to group 2. Statistical processing was performed using Statistica for Windows version 6.0. Results. Patients had tendency to increased body mass index (BMI) in the DM group, but without significant differences. The results of the 6-minute walk test showed a tendency to decreased distance in the group of patients with diabetes. There was an increase in leptin levels and a decrease in adiponectin in patients with diabetes without significant differences. Levels of IL-6, glycosylated hemoglobin, and Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) index were significantly higher in the cohort of patients with diabetes (p <0.05). Conclusions. Women aged 40–60 years with LVDD with hypertension, class I–III obesity and type 2 diabetes mellitus differ from similar cohorts of patients without diabetes with a tendency to increased BMI levels, leptinemia, and decrease in distance of 6-minute walk test, LV ejection fraction and blood adiponectin level; they have significantly higher blood levels of interleukin-6, glycosylated hemoglobin (HbA1c) and HOMA-IR; indicators of diastolic function in the group of patients with diabetes tend to worsen the parameters of diastolic filling of the LV even in grade 1 DD.

Takotsubo cardiomyopathy associated with the administration of intranasal phenylephrine/lignocaine for epistaxis

1as a reversible form of left ventricular dysfunction, followed up by a case series in five patients. Although previously considered rare, over the past two decades there has been a marked rise in the number of publications relating to TTC, with the current estimation being that the condition accounts for over 1% of all cases of acute coronary syndrome presentations. The condition is defined by transient, reversible left ventricular systolic dysfunction with no macrovascular coronary artery disease, as confirmed by coronary angiography. Epidemiologically, postmenopausal women seem to be at highest risk, however the condition has been seen in multiple different patient populations. Although classically described in the setting of acute emotional or physical stress and associated with catecholamine overstimulation, exogenous administration of sympathomimetic agents has been reported to cause stress induced left ventricular dysfunction, particularly when administered intravenously. A 67 year old lady with a background of hypertension, Raynaud’s phenomenon and gastroparesis requiring PEJ (percutaneous endoscopic jejunostomy) feeding, presented with persistent recurrent epistaxis to the emergency department on a Friday evening. She had previously had episodes of nitrate responsive angina over the past decade, and previous coronary angiography in 2008 had demonstrated no significant lesions, with a diagnosis of presumptive microvascular disease noted in the history. She also had a history of ventricular tachycardia, for which she had been treated with flecainide, with a structurally normal heart on previous echocardiography, and no other significant cardiovascular risk factors.

Late cardiac effects of chemotherapy in breast cancer survivors treated with adjuvant doxorubicin: 10-year follow-up.

Doxorubicin (Dox), a mainstay of adjuvant breast cancer treatment, is associated with cardiac toxicity in the form of left ventricular dysfunction (LVD), LV diastolic dysfunction, or LV systolic dysfunction. Study objectives were to evaluate the prevalence of LVD in long-term breast cancer survivors treated with Dox and determine if brain-type natriuretic peptide (BNP) may help identify patients at risk for LVD. Patients who participated in prospective clinical trials of adjuvant Dox-based chemotherapy for breast cancer with a baseline left ventricular (LV) ejection fraction evaluation from 1999 to 2006 were retrospectively identified from the St Vincent's University Hospital database. Patients were invited to undergo transthoracic echocardiography, BNP analysis, and cardiovascular (CV) risk factor assessment. LVDD was defined as left atrial volume index >34 mL/m(2) and/or lateral wall E prime <10 m/s, and LVSD as LVEF <50 %. Of 212 patients identified, 154 participated, 19 patients had died (no cardiac deaths), and 39 declined. Mean age was 60.7 [55:67] years. A majority of the patients (128, 83 %) had low CV risk (0/1 risk factors), 21 (13.6 %) had 2 RFs, and 5 (3.2 %) ≥3 RFs. BMI was 27.2 ± 4.9 kg/m(2). Median Dox dose was 240 mg/m(2) [225-298]; 92 patients (59.7 %) received ≤240 mg/m(2) and 62 (40.3 %) > 240 mg/m(2). Baseline LVEF was 68.2 ± 8 %. At follow-up of 10.8 ± 2.2 years, LVEF was 64.4 ± 6 %. Three (1.9 %) subjects had LVEF <50 % and one (0.7 %) had LVDD. Dox >240 mg/m2 was associated with any LVEF drop. BNP levels at follow-up were 20.3 pg/ml [9.9-36.5] and 21.1 pg/ml [9.8-37.7] in those without LVD and 61.5 pg/ml [50-68.4] in those with LVD (p = 0.04). Long-term prospective data describing the impact of Dox on cardiotoxicity are sparse. At over 10 years of follow-up, decreases in LVEF are common, and dose related, but LVD as defined is infrequent (2.6 %). Monitoring with BNP for subclinical LVD needs further evaluation.

Elevated ejection-phase myocardial wall stress in children with chronic kidney disease.

Myocardial wall stress (MWS) is thought to be the mechanical stimulus to ventricular hypertrophy. The objective of this study was to examine whether MWS is elevated in children with chronic kidney disease (CKD) who are at high risk of developing adverse cardiovascular events related to left ventricular (LV) hypertrophy. MWS, a function of left ventricular pressure, myocardial wall volume, and cavity volume, was obtained using carotid tonometry to estimate ventricular pressure and 2-dimensional transthoracic echocardiographic wall-tracking to obtain LV cavity and wall volumes. Ninety-two children (50 boys) aged 11.2±3.2 (mean±SD) years, including healthy controls (n=16), and those with CKD disease divided into 3 groups according to estimated glomerular filtration rate (mL/min per 1.73 m2) >90 (CKD 1, n=26), 60 to 90(CKD 2, n=23), and <60 (CKD≥3, n=27) were studied. There was no significant difference in age, height, weight, central or peripheral blood pressure, LV mass, or mass index in the 4 study groups. By contrast, peak, mean, and end-systolic MWS were higher in children with CKD and increased across stages of CKD (peak MWS, 338.8±18.5 and 397.5±14.3 s/cm2 in controls and CKD≥3, respectively; P=0.01). Higher systolic MWS was explained by a form of LV dysfunction whereby dynamic values of the ratio of wall volume/cavity size during systole were lower in children with CKD than in those without (P=0.001). Children with CKD exhibit blood pressure–independent LV dysfunction which results in increased systolic MWS and which may predispose to LV hypertrophy in later life.

Management of Diastolic Heart Failure

The diastolic heart failure also referred to as heart failure with preserved left ventricular systolic function (preserved ejection fraction). The difference between systolic and diastolic HFs is a pathophysiological one and isolated forms of left ventricular dysfunction are rarely observed. In diastolic HF left ventricular systolic function is normal or only slightly impaired, and the typical manifestations of HF result from increased filling pressure caused by impaired relaxation and compliance of the left ventricle. The management should include antihypertensive treatment, maintenanceof the sinus rhythm, prevention of tachycardia, venous pressure reduction, prevention of myocardial ischemia and prevention of diabetes mellitus. Treatment of diastolic HF is aimed to stop the progression of the disease, relieve its symptoms, eliminate exacerbations and reduce the mortality. The predisposing factors for diastolic dysfunction include elderly age, female sex, obesity, coronary artery disease, hypertension and diabetes mellitus. The European Society of Cardiology specifies the type of therapy in diastolic HF based on: angiotensin converting enzyme inhibitors, angiotensin receptor blockers, beta-blockers, non dihydropyridine calcium channel blockers, diuretics.

Bridging to Recovery: Experience with the Wearable Cardioverter Defibrillator in Patients with Tachycardia-Induced Cardiomyopathy

Tachycardia-induced cardiomyopathy (TIC) is considered a reversible form of left ventricular dysfunction. Although patients with TIC are at high risk of sudden cardiac arrest, once the heart rate is under control rapid clinical improvement is expected. Hence, an implantable defibrillator (ICD) may not be an optimal clinical solution before a permanent risk is identified. Moreover, the tachycardia burden (usually of supraventricular origin) makes TIC patients more susceptible to false shocks. Previous studies have reported the effectiveness of a wearable cardioverter defibrillator (WCD) in terminating life-threatening ventricular arrhythmias (VAs).

Using Cardiac Biomarkers and Treating Cardiotoxicity in Cancer

Cardiotoxicity is a frequent and serious adverse effect of both conventional and novel anticancer treatments, affecting patient survival and quality of life. The current standard for cardiac monitoring during cancer therapy, mainly based on left ventricular ejection fraction assessment, detects myocardial damage only when a functional impairment has already occurred, not allowing for early preventive strategies. Measurement of cardiospecific biomarkers has proven to have higher prognostic value than imaging modalities. In particular, cardiac troponin elevation during chemotherapy allows the identification of patients who are more prone to develop myocardial dysfunction and cardiac events during follow-up. In these patients, the use of an angiotensin-converting enzyme inhibitor such as enalapril has shown to be effective in improving clinical outcome, giving the chance for a cardioprotective strategy in a selected population. Once left ventricular dysfunction occurs, heart failure therapies currently used for other forms of left ventricular dysfunction, particularly angiotensin-converting enzyme inhibitors and β-blockers, seem to be effective. However, their use in cancer patients is still undervalued.

Cardiac thrombus and conduction disorder in takotsubo cardiomyopathy

Takotsubo cardiomyopathy is a reversible form of left ventricular dysfunction with an apparently benign natural history after left ventricular recovery. Rarely there are complications such as arrhythmias and apical thrombus. We describe a case of takotsubo cardiomyopathy complicated with apical thrombus and persistent complete atrioventricular block after improvement of left ventricular wall motion.

Cardiac thrombus and conduction disorder in takotsubo cardiomyopathy

Takotsubo cardiomyopathy is a reversible form of left ventricular dysfunction with an apparently benign natural history after left ventricular recovery. Rarely there are complications such as arrhythmias and apical thrombus. We describe a case of takotsubo cardiomyopathy complicated with apical thrombus and persistent complete atrioventricular block after improvement of left ventricular wall motion.

Assessment of left ventricular systolic function and diastolic filling characteristics in patients with pulmonary thromboembolism

The purpose of the present study aimed to evaluate the left ventricular systolic function and diastolic filling characteristics in pulmonary thromboembolism (PTE). A total of 102 patients with PTE, including acute or acute on chronic PTE, were consecutively recruited from January of 2006 to December of 2010. The patients [53 males and 49 females; age (64 ± 14) years, range 23 - 85 years] all underwent Doppler echocardiographic assessment before thrombolytic therapy or within 24 h of hospital admission to the emergency intensive care unit of Beijing Anzhen hospital. Fifty-one age- and gender-matched healthy controls [29 males and 22 females; age (61 ± 9) years, range 31-79 years] were recruited from the Health Center. One hundred and sixty age- and gender-matched coronary artery disease (CAD) patients [90 males and 70 females, age (61 ± 11) years, range 29 - 81 years] with positive coronary artery angiography were also included as controls during the period of January of 2009 through December of 2010. Trans-thoracic Doppler echocardiography was used to assess the trans-mitral filling pattern and left ventricular systolic function in all the subjects. The trans-mitral blood flow peak of early (E) wave less than that of the auricular (A) wave, or the ratio of E/A greater than 2, were defined as abnormal left ventricular diastolic filling. Left ventricular ejection fraction (LVEF) greater than 50% was defined as preserved systolic function. The prevalence of abnormal left ventricular diastolic filling and systolic dysfunction were compared with Chi-square test between the PTE patients and the 2 control groups. Tricuspid regurgitation was identified in 72.5% (74/102) of the 102 PTE patients, abnormal left ventricular diastolic filling was detected in 77.5% (79/102) of the PTE patients, and 95.1% (97/102) of the PTE patients had preserved left ventricular systolic function with LVEF of > 50%. Further analysis revealed that the abnormal left ventricular diastolic filling was more frequent in PTE patients with CAD and/or hypertension than in other PTE patients (χ(2) = 5.280, P < 0.05), 85.2% (52/61) and 65.9% (27/41), respectively. Overall, the prevalence of abnormal left ventricular diastolic filling in PTE patients (77.5%, 79/102) was significantly higher than that in healthy controls (25.5%, 13/51, χ(2) = 38.300, P < 0.001), and the fraction of left ventricular systolic dysfunction was significantly lower (4.9%, 5/102) than that in CAD patients (29.4%, 47/160, χ(2) = 23.450, P < 0.001). In the PTE patients with neither CAD nor hypertension, the abnormal left ventricular diastolic filling was still more frequent (65.9%, 27/41) than in healthy controls (25.5%, 13/51, χ(2) = 15.070, P < 0.001), but there was no significant difference when compared with that in CAD patients (73.8%, 118/160, χ(2) = 1.013, P > 0.05). The results strongly suggest that abnormal left ventricular diastolic filling constitutes a common and a major form of left ventricular dysfunction in PTE patients. It indicates that enhanced alertness to and early identification of abnormal left ventricular diastolic filling may play an important role in improving prognosis for PTE.

Familial Occurrence of Peripartum Cardiomyopathy Presages a Genetic Rather Than an Environmental Cause

Peripartum cardiomyopathy (PPCM) is an uncommon form of left ventricular dysfunction associated with pregnancy and triggered by a number of obstetric factors including pre-eclampsia, plural gestations and multiparity. PPCM is the most frequent cause of pregnancy-related maternal death. Although the clinical outcome of PPCM has been determined, its patho-etiology has not been elucidated. Two recent studies have demonstrated for the first time in a small proportion of patients, convincing evidence of a genetic predisposition for PPCM, activated by modifier genes responding to biochemical and hemodynamic signals during mid to late pregnancy.

Relationship between burden of premature ventricular complexes and left ventricular function

Frequent idiopathic premature ventricular complexes (PVCs) can result in a reversible form of left ventricular dysfunction. The factors resulting in impaired left ventricular function are unclear. Whether a critical burden of PVCs can result in cardiomyopathy has not been determined. The objective of this study was to determine a cutoff PVC burden that can result in PVC-induced cardiomyopathy. In a consecutive group of 174 patients referred for ablation of frequent idiopathic PVCs, the PVC burden was determined by 24-hour Holter monitoring, and transthoracic echocardiograms were used to assess left ventricular function. Receiver-operator characteristic curves were constructed based on the PVC burden and on the presence or absence of reversible left ventricular dysfunction to determine a cutoff PVC burden that is associated with left ventricular dysfunction. A reduced left ventricular ejection fraction (mean 0.37 +/- 0.10) was present in 57 of 174 patients (33%). Patients with a decreased ejection fraction had a mean PVC burden of 33% +/- 13% as compared with those with normal left ventricular function 13% +/- 12% (P <.0001). A PVC burden of >24% best separated the patient population with impaired as compared with preserved left ventricular function (sensitivity 79%, specificity 78%, area under curve 0.89) The lowest PVC burden resulting in a reversible cardiomyopathy was 10%. In multivariate analysis, PVC burden (hazard ratio 1.12, 95% confidence interval 1.08 to 1.16; P <.01) was independently associated with PVC-induced cardiomyopathy. A PVC burden of >24% was independently associated with PVC-induced cardiomyopathy.

Prevalence and Clinical Characteristics of Right Ventricular Dysfunction in Transient Stress Cardiomyopathy

Transient stress cardiomyopathy (TSC) is a cause of reversible left ventricular (LV) dysfunction that is increasingly recognized. Reports to date have focused primarily on LV involvement, with little attention paid to associated right ventricular (RV) dysfunction. With other forms of LV dysfunction, RV involvement has been shown to confer an adverse prognosis. Prevalence, clinical characteristics, and short-term prognosis of RV dysfunction in TSC remain ill-defined. Presenting echocardiograms of 40 patients with TSC were reviewed. RV function was assessed by evaluating regional wall motion and calculating a wall motion score index (WMSI). RV dysfunction was defined as a WMSI >1.0. Clinical and demographic characteristics of patients with and without RV dysfunction were compared. RV dysfunction was identified in 27% of patients (11 of 40). RV WMSI was 1.20 +/- 0.30 for the entire cohort compared with 1.72 +/- 0.30 for those with RV dysfunction (p <0.05). In each case with RV dysfunction, regional wall motion abnormalities involved the apex and spared the base. Patients with RV dysfunction had higher B-type natriuretic peptide levels, higher pulmonary artery systolic pressures, and longer hospital stays. RV dimensions, clinical characteristics, electrocardiographic findings, other biomarkers, and in-hospital complications were similar. In conclusion, RV wall motion abnormalities, predominantly involving the apex and sparing the base, occur in slightly >1/4 of cases of TSC. Although associated with higher B-type natriuretic peptide levels, higher pulmonary artery systolic pressures, and longer hospital stays, RV dysfunction was not associated with significant differences in short-term cardiac morbidity or increased early mortality.

Regional myocardial hybernation detected by low-dose dobutamine stress MRI in minipigs with prolonged left ventricular dyssynchronous contraction

Purpose: Neuregulin-1 (NRG-1) is a paracrine growth factor released from endothelial cells in the heart. It stimulates ErbB2 and ErbB4 receptors on cardiomyocytes. Paracrine NRG-1 signalling in the myocardium is activated after exposure to anthracyclines and protects against the development of toxic cardiomyopathy. Conversely, inhibition of NRG-1 signalling after administration of trastuzumab, a monoclonal anti-ErbB2 antibody, exacerbates anthracycline-induced left ventricular (LV) dysfunction. The role of NRG-1 and ErbB activation in other forms of LV dysfunction is still incompletely understood. In this study, we hypothesized that myocardial NRG-1/ErbB signalling is activated during overdrive pacing-induced heart failure. Methods: Nineteen male beagle dogs with pacing-induced heart failure (HF) over 4 to 7 weeks underwent weekly echocardiograms and endomyocardial biopsies. Relative mRNA expression of target genes was measured with real-time RT-PCR. Phosphorylated ErbB2 and ErbB4 were measured by immunoprecipitation and Western blotting after sacrifice in 6 normal dogs, in 6 dogs with moderate HF (4 weeks of pacing) and in 7 dogs with overt congestive HF (7 weeks of pacing). Results: Rapid right ventricular pacing increased LV end-diastolic volume (64±4.3 ml/m2 at baseline and 113±7.2 ml/m2 at week 7, p<0.001) and decreased LV ejection fraction (67±1.6% at baseline and 37±2.6% at week 7, p<0.001). Over the same time course, ventricular NRG-1 mRNA expression increased 4-fold (p<0.01) and expression of a proteolytic enzyme promoting NRG-1 release, ADAM19, increased 2-fold (p<0.05). Left ventricular ErbB2 and ErbB4 receptors showed increasing degrees of overall and site-specific tyrosine phosphorylation over time. ErbB2 receptors underwent truncation exclusively in myocardium of dogs with moderate and severe HF, leading to the formation of a 95 kDa membrane-bound receptor remnant. Conclusions: Pacing-induced cardiomyopathy is accompanied by activation of myocardial NRG-1/ErbB signalling, as shown by increased NRG-1 expression and phosphorylation of ErbB2 and ErbB4 receptors in the LV. As a novel and intriguing observation, we describe the appearance of a truncated form of ErbB2 in the myocardium. In breast tumours, expression of this form is known to be associated with constitutive receptor activity and with poor cancer outcome. Whether, in analogy, ErbB2 truncation in the myocardium can be interpreted as a further manifestation of activated ErbB2 signalling remains to be confirmed, but may have interesting clinical applications.

A rare case of tako-tsubo cardiomyopathy with variable forms of left ventricular dysfunction: A new entity

We report a rare case of an 83-year-old woman with tako-tsubo cardiomyopathy, who presented with variable forms of left ventricular dysfunction during her clinical course. The distribution regional wall-motion abnormalities of the left ventricle on echocardiography had changed from a mid-ventricular ballooning type to the apical ballooning type 3 days from the onset. We suggest that these findings may indicate a new or variant entity of tako-tsubo cardiomyopathy.

Tako‐tsubo Cardiomyopathy Complicating Left Atrial Radiofrequency Ablation

Two female patients undergoing left atrial radiofrequency catheter ablation developed Tako-tsubo cardiomyopathy. This reversible form of left ventricular dysfunction is known to occur under conditions associated with marked sympathetic nervous activation. Radiofrequency catheter ablation in the left atrium can damage autonomic ganglionated plexi, leading to vagal withdrawal, thus resulting in enhanced sympathetic tone. Tako-tsubo cardiomyopathy has not been previously described following radiofrequency catheter ablation.

Rate control in atrial fibrillation: choice of treatment and assessment of efficacy.

The clinical relevance and high social costs of atrial fibrillation have boosted interest in rate control as a cost-effective alternative to long-term maintenance of sinus rhythm (i.e. rhythm control). Prospective studies show that rate control (coupled with thromboembolic prophylaxis) is a valuable treatment option for all forms of atrial fibrillation. The rationale for rate control is that high ventricular rates, frequently found in atrial fibrillation, lead to haemodynamic impairment, consisting of a variable combination of loss of atrial kick, irregularity in ventricular response and inappropriately rapid ventricular rate, depending on the type of underlying heart disease. Long-term persistence of tachycardia at a high ventricular rate can lead to various degrees of ventricular dysfunction and even to tachycardiomyopathy-related heart failure. Identification of this reversible and often concealed form of left ventricular dysfunction can permit effective management by rate (or rhythm) control. Although acute rate control (to reduce ventricular rate within hours) is still often based on digoxin administration, for patients without left ventricular dysfunction, calcium channel antagonists or beta-adrenoceptor antagonists (beta-blockers) are generally more appropriate and effective. In chronic atrial fibrillation, long-term rate control (to reduce morbidity/mortality and improve quality of life) must be adapted to patients' individual characteristics to grant control during daily activities, including exercise. According to current guidelines, the clinical target of rate control should be a ventricular rate below 80-90 bpm at rest. However, in many patients, assessment of the appropriateness of different drugs should include exercise testing and 24h-Holter monitoring, for which specific guidelines are needed. In practice, rate control is considered a valid alternative to rhythm control. Recent prospective trials (e.g. the Pharmacological Intervention in Atrial Fibrillation [PIAF] and the Atrial Fibrillation Follow-up Investigation of Rhythm Management [AFFIRM] trials) have shown that in selected patients, rate control provides similar benefits, more economically, in terms of quality of life and long-term mortality. The choice of a rate control medication (digoxin, beta-blockers, calcium channel antagonists or possibly amiodarone) or a non-pharmacological approach (mainly atrioventricular node ablation coupled with pacing) must currently be based on clinical assessment, which includes assessing the presence of underlying heart disease and haemodynamic impairment. Definite guidelines are required for each different subset of patients. Rate control is particularly tricky in patients with heart failure, for whom non-pharmacological options can also be considered. The preferred pharmacological options are beta-blockers for stabilised heart failure and digoxin for unstabilised forms.

Myocardial injury and left ventricular performance after subarachnoid hemorrhage.

Electrocardiographic abnormalities and elevations of the creatine kinase myocardial isoenzyme (CK-MB) occur frequently after subarachnoid hemorrhage. In some patients, a reversible and presumably neurogenic form of left ventricular dysfunction is demonstrated by echocardiography. It is not known whether cardiac injury of this type adversely affects cardiovascular hemodynamic performance. We retrospectively studied 72 patients admitted to our neuro-ICU for aneurysmal subarachnoid hemorrhage over a 2.5-year period. We selected patients who met the following criteria: (1) CK-MB levels measured within 3 days of onset, (2) pulmonary artery catheter placed, (3) echocardiogram performed, and (4) no history of preexisting cardiac disease. Hemodynamic profiles were recorded on the day after surgery (n=67) or on the day of echocardiography (n=5) if surgery was not performed (mean, 3. 3+/-1.7 days after onset). The severity of cardiac injury was classified as none (peak CK-MB <1%, n=36), mild (peak CK-MB 1% to 2%, n=21), moderate (peak CK-MB >2%, n=6), or severe (abnormal left ventricular wall motion, n=9). Abnormal left ventricular wall motion occurred exclusively in patients with peak CK-MB levels >2% (P<0.0001), poor neurological grade (P=0.002), and female sex (P=0.02). Left ventricular stroke volume index and stroke work index were elevated above the normal range in patients with peak CK-MB levels <1% and fell progressively as the severity of cardiac injury increased, with mean values for patients with abnormal wall motion below normal (both P<0.0001 by ANOVA). Cardiac index followed a similar trend, but the effect was less pronounced (P<0.0001). Using forward stepwise multiple logistic regression, we found that thick subarachnoid clot on the admission CT scan (odds ratio, 1.9; 95% confidence interval [95% CI], 1.0 to 3.4; P=0.04) and depressed cardiac index (odds ratio, 2.1; 95% CI, 1.0 to 4.1; P=0.04) were independent predictors of symptomatic vasospasm. Myocardial enzyme release and echocardiographic wall motion abnormalities are associated with impaired left ventricular performance after subarachnoid hemorrhage. In severely affected patients, reduction of cardiac output from normally elevated levels may increase the risk of cerebral ischemia related to vasospasm.