Search

Accumulation of medical knowledge related to diagnosis and management over the last 5-6 decades has altered the course of diseases, improved clinical outcomes and increased survival. Thus, it has become difficult for the practicing physician to evaluate the long-term effects of a particular therapy on survival of an individual patient. Further, the approach by each physician to an individual patient with the same disease is not always uniform. In an attempt to assist physicians in applying newly acquired knowledge to patients, clinical practice guidelines were introduced by various scientific societies. Guidelines assist in facilitating the translation of new research discoveries into clinical practice; however, despite the improvements over the years, there are still several issues related to guidelines that often appear ‘lost in translation'. Guidelines are based on the results of randomized clinical trials, other nonrandomized studies, and expert opinion (i.e. the opinion of most members of the guideline committees). The merits and limitations of randomized clinical trials, guideline committees, and presentation of guidelines will be discussed. In addition, proposals to improve guidelines will be presented.

We aimed to evaluate the effect of continuous positive airway pressure (CPAP) therapy on blood pressure (BP) and arterial stiffness in hypertensive patients with obstructive sleep apnea (OSA).We studied 38 hypertensive patients who suffered from severe OSA. Ambulatory BP measurement was performed at baseline and after at least 3 months of uninterrupted CPAP therapy. In 19 of these patients, we also measured pulse wave velocity (PWV) at baseline, after the first night of CPAP therapy and at 3 months. Fifteen normotensive subjects without OSA comprised the control group.CPAP therapy reduced systolic BP from 141.5 ± 12.1 to 133.5 ± 9.7 mmHg (p = 0.007) and diastolic BP from 87.8 ± 6.8 to 83 ± 5.4 mmHg (p = 0.004). CPAP also reduced the PWV from 8.81 ± 1.4 to 8.18 ± 1 m/s after the first night of CPAP therapy (p = 0.003) and to 7.37 ± 1 m/s at 3 months (p = 0.007).To the best of our knowledge, this is the first study demonstrating that CPAP therapy in hypertensive patients with OSA improves arterial stiffness from the first night and that this favorable effect is maintained for at least 3 months of CPAP use. A reduction in BP was also observed, even though BP control was not always achieved.

Old age, female gender, hypertension (HTN), cardiac ischaemia, and arterial stiffness (AS) are the main determinants of a stiff heart, diastolic dysfunction (DD), and finally heart failure with preserved ejection fraction (HFpEF); however, several cardiac or extra-cardiac pathologies may also be involved. The combined ventricular-arterial stiffening (abnormal left ventricle-arterial coupling) is the main determinant of the increased prevalence of HFpEF in elderly persons, particularly women, and in younger subjects with HTN. Hospitalization and mortality rates in patients with HFpEF are similar to those of patients with heart failure with reduced EF (HFrEF). However, although the prognosis of HFrEF has improved over time, the optimal treatment of HFpEF remains unclear, because of the differences in the pathophysiology of the two syndromes. A number of new drugs have shown promise but they will not be commercially available for several years. For the time being, aggressive treatment of non-cardiac comorbidities is the only option available for the management of HFpEF. Treatment of anaemia, sleep disorders, chronic kidney disease, non-alcoholic fatty liver disease, atrial fibrillation, diabetes mellitus, and judicious use of diuretics are effective to some degree. Statin treatment deserves special attention, regardless of the presence of dyslipidaemia, because it has been shown, mainly in small studies, post hoc analyses, and in a large recent meta-analysis, that it is related to an improved quality of life and a reduction in HF-related mortality. We urgently need to utilize these recourses to relieve a substantial number of patients suffering from HFpEF, a disease with an ominous prognosis.

Coronary atherosclerosis is a long lasting and continuously evolving disease with multiple clinical manifestations ranging from asymptomatic to stable angina, acute coronary syndrome (ACS), heart failure (HF) and sudden cardiac death (SCD). Genetic and environmental factors contribute to the development and progression of coronary atherosclerosis. In this review, current knowledge related to the diagnosis and management of coronary atherosclerosis based on pathophysiologic mechanisms will be discussed. In addition to providing state-of-the-art concepts related to coronary atherosclerosis, special consideration will be given on how to apply data from epidemiologic studies and randomized clinical trials to the individual patient. The greatest challenge for the clinician in the twenty-first century is not in absorbing the fast accumulating new knowledge, but rather in applying this knowledge to the individual patient.

Left ventricular hypertrophy (LVH) with intraventricular septum thickness (IVST) between 1.2 and 1.5 cm in athletes represents a "gray zone" between physiologic adaptation and mild hypertrophic cardiomyopathy (HCM). Various echo and laboratory parameters have been reported till now in the literature to discriminate the "gray zone" entities. Aim of this study was to assess the efficacy of these "classic" parameters in differentiating physiologic LVH in athletes from mild HCM in a highly selected population. Nine highly trained athletes with IVST (1.28 ± 0.07 cm), 9 patients with mild HCM (1.38 ± 0.11 cm), and 26 athletes without LVH (1.06 ± 0.09 cm; P 0.0005) underwent echocardiographic study, cardiopulmonary treadmill exercise stress test, and brain natriuretic peptide (BNP) measurement before and after exercise. Among all parameters tested, 7 were found to significantly differ between "gray zone" groups. After bootstrapping analysis, it was found that athletes with left ventricular end-diastolic diameter4.74 cm, mitral deceleration time200 ms, isovolumic relaxation time94 ms, tricuspid E/A 1.63, septum Em 9.5 cm/sec, relative wall thickness0.445, and a BNP value at rest9.84 pg/mL had a greater possibility for having underlying cardiomyopathy. A 10-point score based on these parameters showed accuracy (area under the curve = 0.958 [95%CI: 0.738-1.0; P = 0.00005, standard error = 0.0342]) for revealing HCM in a gray zone athletic population. Differentiation of adaptive LVH versus HCM in a gray zone population could be facilitated by recognition of certain features referring to LV dimensions, diastolic function, and BNP.

Ranolazine, an antianginal agent with antiarrhythmic properties, prevents atrial fibrillation (AF) in patients with acute coronary syndrome. In experimental models, the combination of ranolazine and amiodarone has marked synergistic effects that potently suppress AF. Currently, the clinical effect of the ranolazine-amiodarone combination for the conversion of AF is unknown. This prospective randomized pilot study compared the safety and efficacy of ranolazine plus amiodarone versus amiodarone alone for the conversion of recent-onset AF. We enrolled 51 consecutive patients with AF (48-hour duration) eligible for pharmacologic cardioversion. Patients (33 men, 63 ± 8 years of age) were randomized to intravenous amiodarone for 24 hours (group A, n = 26) or to intravenous amiodarone plus oral ranolazine 1,500 mg at time of randomization (group A + R, n = 25). The 2 groups were well balanced with respect to clinical characteristics and left atrial diameter. Conversion within 24 hours (primary end point) was achieved in 22 patients (88%) in group A + R versus 17 patients (65%) in group A (p = 0.056). Time to conversion was shorter in group A + R than in group A (9.8 ± 4.1 vs 14.6 ± 5.3 hours, p = 0.002). According to Cox regression analysis, left atrial diameter and A + R treatment were the only independent predictors of time to conversion (hazard ratio 5.35, 95% confidence interval 2.37 to 12.11, p0.001; hazard ratio 0.81, 95% confidence interval 0.74 to 0.88, p0.001, respectively). There were no proarrhythmic events in either group. In conclusion, addition of ranolazine to standard amiodarone therapy is equally safe and appears to be more effective compared to amiodarone alone for conversion of recent-onset AF.

Background: Preinfarction angina (PA) is a clinical analogue of ischemic preconditioning that improves postinfarct prognosis. Data concerning the association of PA with post infarction left ventricular (LV) remodeling and LV diastolic function are limited. We aimed to evaluate this association in patients with acute myocardial infarction (AMI) in the modern clinical era of widespread use of revascularization and antiremodeling medical treatment. Methods: We studied 53 patients with anterior AMI who underwent complete reperfusion and received up to date antiremodeling medical treatment. LV remodeling, systolic and diastolic function were assessed using 2D echocardiography at baseline and 6 at months follow-up. Patients were divided into two groups regarding the presence or absence of PA. Results: LV remodeling at follow-up was less frequent in the PA group (25 vs. 55 %, P

Background: The role of brain natriuretic peptide (BNP) in differentiating the athlete’s heart from maladaptive cardiac hypertrophy is unclear. Methods: To address this issue, an integrated M mode, two-dimensional B mode and Doppler echocardiographical study were performed and plasma BNP levels were measured in 25 strength athletes, 25 patients with established hypertrophic cardiomyopathy (HCM) and 25 healthy volunteers. Results: Among athletes, BNP levels correlated negatively with the total training time (r = −0.79, p = 0.002) and positively with ejection fraction (r = 0.58, p = 0.049) and fractional shortening (r = 0.57, p = 0.049). A BNP cut-off value of 11.8 pg/ml had 88% specificity and 74% negative predictive value for the exclusion of HCM. Conclusions: Brain natriuretic peptide might be useful as a preparticipation screening test in athletes.

Atrial fibrillation (AF) is a common arrhythmia with evidence of genetic susceptibility. The rs2200733 single-nucleotide polymorphism (SNP) in a non-coding region on chromosome 4q25 has been associated with AF. The purpose of this case-control study was to examine the possible association of the rs2200733 polymorphism with AF in the Greek population.A total of 295 individuals, 167 AF patients and 128 controls, were genotyped for the presence of the rs2200733 polymorphism using a polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLPs) method.The T/T genotype and the T allele were detected more frequently in patients with AF compared to controls (13.2% vs. 2.3%, p=0.001, and 29.6% vs. 17.9%, p=0.001), suggesting that the rs2200733 polymorphism increases susceptibility to AF in the Greek population. In a multivariate stepwise analysis that included many conventional precipitating factors for AF, T/T genotype and left atrium (LA) diameter were the only independent predictors of AF (OR 1.74, 95% CI: 1.40-2.98, p=0.005, and OR 2.88, 95% CI: 1.835.62, p0.001, respectively). A trend of association was observed between the T/T genotype and lone AF (p=0.08).Our results suggest that SNP rs2200733 confers a significant risk of AF in the Greek population, providing further support to the previously reported association between AF and rs2200733 polymorphism on chromosome 4q25.

Background The aim of this study was to investigate the systolic and diastolic properties of the right cardiac chambers (the right ventricle and right atrium) among different subsets of athletes to unveil potential variations in right ventricular and right atrial remodeling secondary to different training modes. Methods A cohort of Caucasian male top-level athletes ( n = 108; 80 endurance athletes [EAs], mean age, 31.2 ± 10.4 years; 28 strength-trained athletes [SAs], mean age, 27.4 ± 5.7 years) and untrained controls ( n = 26; mean age, 26.6 ± 5.6 years) ( P = .327) were prospectively enrolled. Conventional echocardiographic parameters, including transtricuspid inflow, Doppler tissue imaging, and two-dimensionally derived peak systolic longitudinal strain and strain rate indices of the right ventricle and right atrium, were calculated. Results EAs had greater internal right ventricular and right atrial dimensions compared with SAs and controls. There were no significant differences concerning strain between groups (−23.1 ± 3.7% in EAs vs −25.1 ± 3.2% in SAs vs −23.1 ± 3.5% in controls, P = .052), with SAs presenting higher global systolic strain rates (−1.42 ± 0.22 sec −1 in SAs vs −1.21 ± 0.21 sec −1 in EAs vs −1.2 ± 0.28 sec −1 in controls, P = .016), as well as greater right atrial strain rate systolic and diastolic components. Training volume (highly vs moderately trained athletes) did not significantly influence deformation parameters. No significant differences concerning diastolic transtricuspid inflow and Doppler tissue imaging indices were also noted among different athlete groups and controls. Conclusions Despite the existence of right geometric alterations in athletes participating in different sport disciplines, few meaningful differences in deformation and diastolic function exist.

We present a case of Brugada syndrome in a young patient whose typical ECG pattern was ‘masked’ after ibutilide was administered for atrial flutter cardioversion. Ibutilide, a class III antiarrhythmic agent used for the treatment of atrial fibrillation and flutter, prolongs the action potential duration plateau phase by augmenting the slow component of the inward Na+ current and by blocking the rapid component of the delayed rectifier potassium current. Insights into the pathophysiology of Brugada syndrome and this first-reported action of ibutilide are supplied, providing a plausible scientific basis for the masking effect of ibutilide. Furthermore, issues concerning the safety of ibutilide administration in patients with Brugada syndrome along with the importance of programmed ventricular stimulation and especially short-long-short sequence protocol in inducing ventricular fibrillation in these patients are also discussed.

AIMS: It is unknown as to whether the result of adenosine testing for the diagnosis of sinus node dysfunction (SND) depends on the clinical presentation. We investigated whether syncope or presyncope are associated with a more pronounced sinus nodal inhibition by adenosine in SND.METHODS AND RESULTS: We studied 46 patients with SND, 33 with syncope or presyncope and 13 without such history. Controls were 30 subjects undergoing electrophysiological studies for supraventricular tachycardia or unexplained syncope. We calculated the corrected sinus node recovery time after intravenous adenosine 0.15 mg/kg (ADSNRT) as well as after atrial pacing (CSNRT). Corrected sinus node recovery time values >525 ms were considered abnormal. Corrected sinus node recovery time after adenosine injection was more prolonged in SND patients with syncope or presyncope as compared with those without such history [median: 4900 inter-quartile range (IQR): 920-8560 ms vs. median: 280 IQR: 5-908 ms; P< 0.005]. In SND patients with syncope or presyncope ADSNRT was more prolonged than CSNRT (median: 4900 IQR: 920-8560 ms vs. median: 680 IQR: 359-1650 ms, P< 0.01). In SND patients without syncope or presyncope no statistical difference was noted between ADSNRT and CSNRT (median: 280 IQR: 5-908 ms vs. median: 396 IQR: 270-600 ms, P= 0.80). The sensitivity of CSNRT for SND diagnosis was 57% and the specificity was 100%. A cut-off of 1029 ms for ADSRNT yields the same sensitivity with a specificity of 96.6%.CONCLUSION: In patients with SND syncope or presyncope relate to an exaggerated sinus nodal suppression by adenosine. Prolonged ADSNRT can diagnose cases with severe underlying SND where a more aggressive management strategy is probably warranted. Europace

Strategically chosen tachycardia detection and therapy options targeting non-sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) can efficiently reduce the morbidity related to implantable cardioverter defibrillator (ICD) therapy. We report a case of a 60-year-old woman with ischemic cardiomyopathy who underwent ICD implantation due to frequent episodes of non-sustained VT. In this case, the inappropriate setting for VF detection in addition to the limited flexibility in device programming for tachycardia confirmation led to the rapid exhaustion of all available shock therapies.

Aortic stiffness is increased in patients undergoing hemodialysis (HD), and it is associated with an increased cardiovascular mortality. Among others, aortic stiffness has been correlated with serum markers of inflammation, indicating a role of the immune system in its pathogenesis. The aim of this study was to evaluate the impact of antigen-presenting cell-dependent T-lymphocyte reactivity on aortic stiffness in HD patients.Twenty patients were enrolled in the study. Exclusion criteria were medications or conditions, other than HD, that are known to influence the immune response or aortic stiffness. Antigen-presenting cell-dependent T-lymphocyte reactivity was assessed by cell proliferation of peripheral blood mononuclear cells cultured with or without stimulation with Staphylococcal enterotoxin B (SEB). Cell proliferation was estimated by immunoenzymatic measurement of bromodeoxyuridine uptake. Aortic stiffness was assessed by carotid-femoral pulse wave velocity (PWV) measurement.Linear regression analysis revealed a strong positive relation between carotid-femoral PWV and antigen-presenting cell-dependent T-lymphocyte reactivity, when SEB at concentrations of 1 ng/mL or 10 ng/mL was used as stimulant.The present study confirms that aortic stiffness in HD patients is positively related to antigen-presenting cell-dependent T-lymphocyte reactivity. The greater the ability of the immune system to react to a monocyte-dependent stimulant and, consequently, to provoke an inflammatory response, the greater the stiffness of the aorta. This is in agreement with the observation that aortic stiffness in HD patients is positively related to various serum inflammation markers.

We studied the predictive accuracy and disparities among cineventriculographic ejection fraction, pre-ejection period over left ventricular ejection time (PEP/LVET) obtained from the systolic time intervals and the percent shortening of the internal echocardiographic diameter (% delta D) in assessing left ventricular performance in 453 consecutive patients without valvular heart disease. In 308 patients all three tests were normal, and in 78 patients all three tests were abnormal. Overall agreement (predictive accuracy) among ejection fraction (normal greater than or equal to 57), % delta D (normal greater than or equal to 28%) and PEP/LVET (normal less than or equal to 0.42) was 85%. In 67 patients disparities among the tests as measures of global left ventricular performance were found. The major mechanisms accounting for such disparities were: (a) large segmental contraction abnormalities which selectively distort the % delta D and ejection fraction and (b) diminished isovolumic pressure (less than 45 mmHg) which distorts PEP/LVET. When patients with segmental contraction abnormalities and low isovolumic pressure were excluded the agreement between PEP/LVET and ejection fraction was 97%, ejection fraction and % delta D 98% and PEP/LVET and % delta D 97%. The combined uses of systolic time intervals and echocardiogram minimizes error due to segmental contraction abnormalities and isovolumic pressure. If both PEP/LVET and % delta D are concordant the agreement with ejection fraction is 94% for normal and 99% for abnormal left ventricular function.