Cardiac resynchronization therapy in China

Congestive heart failure (HF) is a major and growing public health problem.The therapeutic approach includes non-pharmacological measures,pharmacological therapy, mechanical devices,and surgery.Despite the benefits of optimal pharmacologic therapy,the prognosis is still not ideal.At this time,cardiac resynchronization therapy (CRT) has gained wide acceptance as an alternative treatment for HF patients with conduction delay. As an innovative,pacemaker-based approach to the treatment of patients with HF,CRT uses a three-lead     

Cardiac involvement in sickle β-thalassemia

Cardiovascular involvement is a leading cause of mortality and morbidity in patients with inherited hemoglobinopathies, but it has not been adequately assessed in sickle β-thalassemia. We evaluated 115 sickle β-thalassemia patients, aged 34 ± 14 years, along with 50 healthy controls, by resting echocardiography. Patients with systolic left ventricular (LV) dysfunction or severe pulmonary hypertension (PHT) also underwent left and right cardiac catheterization and cardiac magnetic resonance imaging (CMR). Left and right chamber dimensions, LV mass, and cardiac index were significantly higher in patients compared to controls (p < 0.001 in most cases). Three patients (2.9%) had reduced LV ejection fraction (<55%); mean LV ejection fraction was significantly lower in patients (p < 0.001). Left and right ventricular systolic tissue Doppler indices and LV diastolic tissue Doppler indices were also impaired in patients. All three patients with systolic LV dysfunction had normal coronary arteries and mild myocardial iron load (CMR T2* values, 18–25 ms). Systolic pulmonary artery pressure was significantly higher in patients compared to controls (p = 0.002); PHT was present in 28 patients (27%), while severe PHT in three (2.9%). In three patients with severe PHT, only one had impaired LV ejection fraction and increased pulmonary wedge pressure. Overall, three patients (2.9%) had a history of heart failure, two with systolic LV dysfunction, and one with severe PHT. Cardiac involvement in sickle β-thalassemia concerns biventricular dilatation and dysfunction along with PHT, leading to congestive heart failure.     

Signaling Pathways Involved in Cardiac Hypertrophy

Cardiac hypertrophy is the heart's response to a variety of extrinsic and intrinsic stimuli that impose increased biomechanical stress. Traditionally, it has been considered a beneficial mechanism; however, sustained hypertrophy has been associated with a significant increase in the risk of cardiovascular disease and mortality. Delineating intracellular signaling pathways involved in the different aspects of cardiac hypertrophy will permit future improvements in potential targets for therapeutic intervention. Generally, there are two types of cardiac hypertrophies, adaptive hypertrophy, including eutrophy (normal growth) and physiological hypertrophy (growth induced by physical conditioning), and maladaptive hypertrophy, including pathologic or reactive hypertrophy (growth induced by pathologic stimuli) and hypertrophic growth caused by genetic mutations affecting sarcomeric or cytoskeletal proteins. Accumulating observations from animal models and human patients have identified a number of intracellular signaling pathways that characterized as important transducers of the hypertrophic response, including calcineurin/nuclear factor of activated T- cells, phosphoinositide 3-kinases/Akt (PI3Ks/Akt) , G protein-coupled receptors, small G proteins, MAPK, PKCs, Gpl30/STAT3, Na /H exchanger, peroxisome proliferator-activated receptors, myocyte enhancer factor 2/histone deacetylases, and many others. Furthermore, recent evidence suggests that adaptive cardiac hypertrophy is regulated in large part by the growth hormone/insulin-like growth factors axis via signaling through the PI3K/Akt pathway. In contrast, pathological or reactive hypertrophy is triggered by autocrine and paracrine neurohormonal factors released during biomechanical stress that signal through the Gq/phosphorlipase C pathway, leading to an increase in cytosolic calcium and activation of PKC.     

Cardiac involvement in Henoch-Schönlein purpura

Cardiac involvement is not regarded as a feature of Henoch‐Schönlein purpura (HSP). We report a patient with HSP who developed significant cardiac symptoms, which resolved with immunosuppression. We review previous cases of HSP with cardiac features, none of which showed a response to treatment, and discuss evidence that cardiac involvement is more common than recognized. The implications for investigation and treatment of this condition are discussed.     

Cardiac stem cell therapy research in China

For more than two decades, the morbidity and mortality of coronary artery disease (CAD) has been increasing rapidly in China. Despite tremendous advances in treatment strate- gies of CAD, heart failure after acute myocardial infarction (AMI) continues to be one of the greatest medical chal- lenges throughout the world. In 1994, Soonpaa and col- leagues first reported the possibility of cardiomyocytes implantation and suggested that intracardiac cell grafting might provide a useful approach…     

Combined Application of Circulatory Assist Devices Following Cardiac Arrest in Patients after Cardiac Surgery

Objectives To evaluate retrospectively the potential benefits of combined utilization of various assisted circulation devices in cardiac arrest patients who did not respond to conventional cardiopulmonary cerebral resuscitation (CPCR). Methods Assisted circulation devices, including emergency cardiopulmonary bypass (ECPB), intra-aortic balloon pump (IABP), and left ventricular assist device (LVAD), were applied to 16 adult patients who had cardiac arrest 82 min-56 h after open heart surgery and did not respond to 20 min or longer conventional CPCR. ECPB was applied to 2 patients, ECPB plus IABP to 8 patients, ECPB plus IABP and LVAD to 6 patients. Results One patient recovered fully and one patient died. Of the other 14 patients, 13 resumed spontaneous cardiac rhythm and one did not; none of them could be weaned from ECPB. Further treatment of the 14 patients with combinations of assisted circulation devices enabled 6 patients to recover. One of the 7 recovered patients died of reoccurring cardiac arrest after 11 days; the other 6 were discharged in good condition and were followed up for 3 -49 months (mean =22 months). Of the 6 discharged patients one suffered cerebral embolism during LVAD treatment, resulting in mild limitation of mobility of the right limbs; the other 5 never manifested any central nervous system complications. There was no late deaths giving a 37.5% (6/16) long-term survival rate. Conclusions ECPB could effectively reestablish blood circulation and oxygen supply, rectify acidosis, and improve internal milieu. The combined utilization of ECPB, IABP, and LVAD reduces the duration of ECPB, improves the incidence of recovery, and offers beneficial alternatives to refractory cardiac arrest patients.     

Cardiac Manifestations of Exhaustive Exercise in Nonathletic Adults: Does Cardiac Fatigue Occur?

The aim of the study was to examine the impact of prolonged exercise leading to physical exhaustion on left ventricular (LV) systolic and diastolic function in untrained healthy subjects, and to examine cardiovascular determinants of exercise performance. Twenty-four nonathletic healthy adults (14 males, 10 females; mean age 42 +/- 11 years) were exercised on a treadmill at 70% of maximal oxygen consumption until physical exhaustion occurred after an average of 84 +/- 39 minutes. Two-dimensional and Doppler echocardiography was performed before and 15 minutes after exercise to assess LV function and geometry, and right ventricular (RV) systolic function. After prolonged exercise, LV ejection fraction and geometry were unchanged, but LV end-diastolic volume, end-systolic volume, and stroke volume decreased. However, due to a higher heart rate (HR), cardiac output increased at 15 minutes post exercise. RV fractional shortening was unchanged. LV peak early to atrial filling velocity ratio decreased post exercise, with an increase in percent atrial contribution. However, less preload-dependent variables of LV diastolic function such as deceleration time, LV inflow propagation rate, mitral annular tissue Doppler and myocardial performance index were unchanged. Preexercise stroke volume and HR were the only predictors (r = 0.86, P < 0.01) of exercise duration. However, age, resting blood pressure, indices of systolic and diastolic function, and LV geometry were not predictors. Prolonged exercise leading to physical exhaustion is not associated with systolic or diastolic dysfunction. Reduced early LV diastolic filling and the relative increase in left atrial contribution seen with prolonged exercise are likely due to preload reduction rather than true diastolic dysfunction.     

N-terminal proBNP—Marker of Cardiac Dysfunction,Fluid Overload,or Malnutrition in Hemodialysis Patients?

Background and objectives: N-terminal probrain type natriuretic peptide (NTproBNP) has been proven to be a valuable biomarker for predicting cardiac events and mortality in the hemodialysis population. However recent reports have suggested that NTproBNP is a marker of volume overload rather than one of cardiac dysfunction. Therefore this study investigated the effect of fluid volume status on NTproBNP.Design, setting, participants, & measurements: Volume status was determined pre- and postdialysis in 72 stable hemodialysis outpatients by multifrequency bioimpedance, and the relationship to NTproBNP values was examined.Results: The mean and median NTproBNP values were 931.9 ± 230 and 242 (90 to 688) pmol/L, respectively. On simple correlation, NTproBNP was associated with markers of volume overload and cardiac dysfunction. However, on logistical regression analysis, the strongest association was with the predialysis ratio of extracellular water/total body water (β 26.6, F29.6, P = 0.000), followed by postdialysis mean arterial blood pressure (β 0.14, F17.1, P = 0.000), dialysate calcium concentration (β −1.19, F14.1, P = 0.002), and change in extracellular fluid volume with dialysis (β 0.27, F7.4, P = 0.009)Conclusions: In this study, NTproBNP was not associated with cardiac dysfunction as assessed by transthoracic echo or nuclear medicine scintigraphy but was dependent on factors associated with volume overload. However, because bioimpedance results can also be affected by malnutrition with loss of cell mass, NTproBNP may be elevated not only in patients with volume overload, but also those with malnutrition.Cardiac disease is prevalent in patients with chronic kidney disease (CKD), particularly those treated by hemodialysis, and is the most common cause of death (1). As patients progress through the stages of CKD, sodium retention typically occurs, leading to expansion of the extracellular fluid volume with the compensatory release of natriuretic peptides due to cardiac wall stretch. In addition to increased secretion, these peptides increase with CKD because they are naturally degraded by renal tubular neutral endopeptidases. As such, cardiac natriuretic peptides are often increased in hemodialysis patients and those with CKD (2). There is a series of natriuretic peptides, and these have been shown to be valuable prognostic biomarkers for cardiac outcomes in patients without kidney failure. Atrial natriuretic peptide (ANP) and its cleavage product N-terminal pro-ANP were the first natriuretic peptides to be studied, but more recently focus has shifted to brain natriuretic peptide (BNP), which is released by the ventricle rather than the atrium. In patients with ESRD on hemodialysis, ANP has been reported to be more responsive to changes in intravascular volume than BNP, whereas BNP appears more reflective of cardiac dysfunction (3). This may be due to the different sizes and half-lives of the peptides, because ANP is cleared during high-flux hemodialysis, with a post dialysis rebound taking some 80 to 100 minutes to re-equilibrate (Mathavakkannan, unpublished data). However, others have shown higher BNP values in volume-overloaded hemodialysis patients without overt cardiac dysfunction (4). Because BNP can also be cleared by high-flux dialysis and has been shown to sequentially fall during the course of a typical dialysis week (5), there has been debate as to whether these cardiac biomarkers are more reflective of fluid volume overload or intrinsic cardiac dysfunction in hemodialysis patients.The situation is somewhat more confusing in that some studies have not specified when blood sampling has been taken, because BNP values will be greatest at the start of the dialysis week after the 72-hour interdialytic interval, and least after the third dialysis session of the week (5), or the time of sampling has varied between study subjects and then compounded by using different methods of assessing fluid volume status. Hence, although BNP appears to be a valuable prognostic biomarker for increased risk of mortality in hemodialysis patients, it is unclear as to whether this is related to volume overload or underlying cardiac dysfunction (6,7).Because previous studies reported that BNP was relatively constant in hemodialysis patients after the midweek dialysis session (5), we introduced post-midweek measurement into clinical practice as a means of standardizing results. To investigate the relationship between N-terminal pro-BNP (NTproBNP), volume status, and cardiac dysfunction, we audited post-midweek dialysis NTproBNP values in a cohort of stable adult hemodialysis patients who had corresponding pre- and postdialysis multifrequency bioimpedance (8) measurements to assess volume status.     

Cardiac resynchronization therapy in congenital heart disease

Cardiac resynchronization therapy (CRT) is an established treatment option for adult patients suffering heart failure due to idiopathic or ischemic cardiomyopathy associated with electromechanical dyssynchrony. There is limited evidence suggesting similar efficacy of CRT in patients with congenital heart disease (CHD). Due to the heterogeneity of structural and functional substrates, CRT implantation techniques are different with a thoracotomy or hybrid approach prevailing. Efficacy of CRT in CHD seems to depend on the anatomy of the systemic ventricle with best results achieved in systemic left ventricular patients upgraded to CRT from conventional pacing. Indications for CRT in patients with CHD were recently summarized in the Pediatric and Congenital Electrophysiology Society (PACES) and the Heart Rhythm Society (HRS) Expert Consensus Statement on the Recognition and Management of Arrhythmias in Adult Congenital Heart Disease and are presented in the text.     

Cardiac Drug Therapy—Considerations in the Elderly

Elderly individuals constitute a majority of patients encountered in current cardiovascular clinical practice. Management of these patients is a clinical challenge owing to a multitude of factors. Although medications such as statins have been shown to reduce cardiovascular mortality in the general population, evidence supporting the use of these drugs in patients greater than 75 years of age is sparse. Furthermore, aging associated changes in organ function and associated comorbidities influence the pharmacokinetics of multiple medications and can potentiate drug toxicity. In this article, we review the evidence behind the use of common cardiovascular medications in elderly patients and discuss pertinent clinical challenges.     

Medication Adherence,Depressive Symptoms,and Cardiac Event–Free Survival in Patients With Heart Failure

BackgroundMedication nonadherence and depressive symptoms predict hospitalization and death in patients with heart failure (HF). Depressed patients have lower medication adherence than nondepressed patients. However, the predictive power of the combination of medication adherence and depressive symptoms for hospitalization and death has not been investigated in patients with HF.ObjectiveThe aim of this study was to explore the combined influence of medication adherence and depressive symptoms for prediction of cardiac event–free survival in patients with HF.Methods and ResultsWe monitored medication adherence in 216 HF patients who completed the Patient Health Questionnaire–9 (PHQ-9) at baseline. Medication adherence was measured objectively with the use of the Medication Event Monitoring System (MEMS). Patients were followed for up to 3.5 years to collect data on cardiac events. Survival analyses were used to compare cardiac event–free survival among groups. The risk of experiencing a cardiac event for patients with medication nonadherence and depressive symptoms was 5 times higher than those who were medication adherent without depressive symptoms. The risk of experiencing a cardiac event for patients with only 1 risk factor was 1.2–1.3 times that of those with neither risk factor.ConclusionsMedication nonadherence and depressive symptoms had a negative synergistic effect on cardiac event–free survival in patients with HF.     

Cardiac Metaplasia: Follow,Treat, or Ignore?

Over the past two decades, evidence has accumulated to challenge the traditional view that cardiac mucosa, which is comprised exclusively of mucus glands, is the normal lining of the most proximal portion of the stomach (the gastric cardia). There is now considerable evidence to suggest that cardiac mucosa develops as a GERD-induced, squamous-to-columnar esophageal metaplasia in some, if not all, cases. Although cardiac mucosa lacks the goblet cells commonly required for a histologic diagnosis of intestinal metaplasia, cardiac mucosa has many molecular features of an intestinal-type mucosa, and appears to be the precursor of intestinal metaplasia with goblet cells. In apparently normal individuals, cardiac mucosa is commonly found in a narrow band, less than 3 mm in extent, on the columnar side of the squamo-columnar junction at the end of the esophagus. A greater extent of cardiac mucosa can be found in GERD patients, and the magnitude of that extent appears to be an index of GERD severity. Presently, the risk of adenocarcinoma imposed by cardiac mucosa is not clear, but appears to be far less than that of intestinal metaplasis with goblet cells. The British Society of Gastroenterology accepts an esophagus lined by cardiac mucosa as a "Barrett's esophagus". However, if one defines Barrett's esophagus as a metaplasia that predisposes to cancer, then only intestinal metaplasia clearly fulfills that criterion at this time. Well-designed, prospective studies are needed to establish the malignant potential of cardiac mucosa.     

Cardiac resynchronization therapy in the elderly heart failure patient

Ms. BP is an 83 year old white female with a long history of congestive heart failure (HF). She is now symptomatic with minimal exertion, has a left ventricular ejection fraction (LVEF) of 20%. Her CHF is due to hypertension (HTN) plus coronary artery disease (CAD) and she is on angiotensin converting enzyme inhibitor (ACEI), furosemide, digoxin, spironolactone, low dose beta blocker and nitrates. Her beta-natriuretic peptide (BNP) in clinic is 3030 pg/ml, heart rate (HR) 100, blood pressure (BP) 89/43. She has rales, jugular venous distention and pedal edema.AnⅡ/Ⅵpansystolic murmur is appreciated over her entire precordium and an S3 is apparent. Her electrocardiogram (ECG) is shown in Figure 1 and reveals sinus tachycardia with a prolonged QRS duration of 159 milliseconds. Her husband brings in a new article about Biventricular pacing and asks you if it will help her. You review her most recent echocardiogram which reveals: LV chamber severely enlarged (LV end diastolic dimension=6.2 cm); Wall motion globally impaired (LVEF=20%); Right ventricle (RV)at normal size with moderate to severe RV dysfunction; Left atrium (LA) moderately to severely enlarged; Right atrium (RA) mildly to moderately enlarged; Moderate to severe mitral regurgitation; Severe tricuspid regurgitation (TR); Estimated cardiac output=3 L/min; Pulmonary artery systolic pressure 89 mmHg; And impaired LV relaxation. Her husband is very socially conscious and you anticipate a bevy of questions. What is your response?     

Does Lethal Reperfusion Injury Exist in Cardiac Surgery?

Journal of Thrombosis and Thrombolysis -     

Chest Pain—Esophageal, Cardiac, or Both?

The esophagus may be the origin of chest pain clinically indistinguishable from that of ischemic heart disease. In some patients the esophageal origin of the pain may only be recognized by pharmacological provocation during manometry. We describe nine patients with chest pain which could be explained by disorders of esophageal motility--diffuse spasm in four, high pressure lower esophageal sphincter in three, and "nutcracker esophagus" in two. Methacholine provoked the pain and manometric abnormalities in five patients who had normal baseline tracings. However, seven patients given methacholine developed ischemic changes on the electrocardiogram. In one patient these were typical of Prinzmetal's variant angina. The manometric and electrocardiographic abnormalities were reversed by intravenous atropine. Ischemic heart disease and esophageal motor disorders may occur concomitantly and pose a dilemma in diagnosis and management.