Myopathy is possibly the most clinically relevant statin-induced side effect.
We report a case of a 63-year-old healthy male with mixed dyslipidemia. He developed bilateral myalgia of the forearms ...with fluvastatin 40 mg/day, pravastatin 20 mg/day, and combination of atorvastatin 10 mg and ezetimibe 10 mg/day. The only hypolipidemic treatment that was tolerable was the combination of pitavastatin 1 mg and ezetimibe 10 mg/day.
Pitavastatin demonstrated less potential for the development of myalgia compared to the so far considered most tolerable statins (i.e., fluvastatin and pravastatin). All the tested statins were used at the lowest approved dose for clinical use.
The combination of pitavastatin 1 mg and ezetimibe appears to be a promising treatment choice for individuals who are intolerant to statin therapy due to muscle complaints.
QRS fragmentation has not been linked with increased mortality in individuals without known cardiac disease. We aimed to investigate the physiological determinants of QRS fragmentation in individuals ...without cardiac disease.
Study participants were 163 (54 athletes, 109 nonathletes) asymptomatic individuals with QRS fragmentation but without cardiac disease. QRS fragmentation was assessed in the supine position after deep inspiration or standing up and during exercise. The changes in QRS fragmentation were evaluated over a median follow-up period of 2.3 (0.8-4.9) years.
The most common lead with QRS fragmentation was III (63.0% in athletes, 61.5% in nonathletes), immediately followed by V1 (50.0%) and aVF (42.6%) in athletes and aVF (55.0%) in nonathletes. QRS fragmentation in V1 was more frequent in athletes compared to nonathletes (
< 0.001). Among athletes, the presence of QRS fragmentation in V1 could be independently predicted by increased RVOTproxi (right ventricular outflow tract proximal diameter indexed to body surface area) (
< 0.001). Among individuals with QRS fragmentation in V1, deep inspiration resulted in disappearance of QRS fragmentation more frequently in nonathletes compared to athletes (100% vs. 20%,
= 0.003). Deep inspiration resulted in disappearance of QRS fragmentation in aVF (
< 0.001). The presence of QRS fragmentation in II or aVF was associated with increased body mass index (BMI) (
= 0.003). Among athletes without QRS fragmentation in V1 at baseline, the appearance of QRS fragmentation in V1 at the end of follow-up was associated with greater training age (
= 0.034). Among individuals with QRS fragmentation in aVF at baseline, the disappearance of QRS fragmentation in aVF at the end of follow-up was associated with greater reduction in BMI (
= 0.008).
The characteristic feature of QRS fragmentation in athletes was the presence of QRS fragmentation in V1, which was associated with RVOTproxi. The persistence of QRS fragmentation in V1 after deep inspiration could serve as a specific marker of exercise-training-related cardiac adaptation. The presence of QRS fragmentation in the leads of the frontal plane was influenced by BMI and respiration phase.
Pathophysiology of Noncardiac Syncope in Athletes Christou, Georgios A; Christou, Konstantinos A; Kiortsis, Dimitrios N
Sports medicine (Auckland),
07/2018, Letnik:
48, Številka:
7
Journal Article
Recenzirano
The most frequent cause of syncope in young athletes is noncardiac etiology. The mechanism of noncardiac syncope (NCS) in young athletes is neurally-mediated (reflex). NCS in athletes usually occurs ...either as orthostasis-induced, due to a gravity-mediated reduced venous return to the heart, or in the context of exercise. Exercise-related NCS typically occurs after the cessation of an exercise bout, while syncope occurring during exercise is highly indicative of the existence of a cardiac disorder. Postexercise NCS appears to result from hypotension due to impaired postexercise vasoconstriction, as well as from hypocapnia. The mechanisms of postexercise hypotension can be divided into obligatory (which are always present and include sympathoinhibition, histaminergic vasodilation, and downregulation of cardiovagal baroreflex) and situational (which include dehydration, hyperthermia and gravitational stress). Regarding postexercise hypocapnia, both hyperventilation during recovery from exercise and orthostasis-induced hypocapnia when recovery occurs in an upright posture can produce postexercise cerebral vasoconstriction. Athletes have been shown to exhibit differential orthostatic responses compared with nonathletes, involving augmented stroke volume and increased peripheral vasodilation in the former, with possibly lower propensity to orthostatic intolerance.
The main dietary source of omega-3 polyunsaturated fatty acids (n-3 PUFA) is fish, which contains eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). In the present manuscript, we aimed to ...review the current evidence regarding the clinical role of n-3 PUFA in the prevention of atrial fibrillation (AF) and the possible underlying mechanisms.
A literature search based on PubMed listings was performed using "Omega-3 fatty acids" and "atrial fibrilation" as key search terms.
n-3 PUFA have been shown to attenuate structural atrial remodeling, prolong atrial effective refractory period through the prevention of reentry and suppress ectopic firing from pulmonary veins. Dietary fish intake has been found to have no effect on the incidence of AF in the majority of studies. Circulating DHA has been consistently reported to be inversely associated with AF risk, whereas EPA has no such effect. The majority of studies investigating the impact of n-3 PUFA supplementation on the incidence of AF following cardiac surgery reported no benefit, though most of them did not use n-3 PUFA pretreatment for adequate duration. Studies using adequate four-week pretreatment with n-3 PUFA before cardioversion of AF showed a reduction of the AF incidence.
Although n-3 PUFA have antiarrhythmogenic properties, their clinical efficacy on the prevention of AF is not consistently supported. Further well-designed studies are needed to overcome the limitations of the existing studies and provide robust conclusions.
We describe a case report of a 30-year-old bodybuilder suffering acute myocardial infarction (AMI). He had been taking stanozolol and testosterone for two months. The coronary angiogram showed high ...thrombotic burden in the left anterior descending artery without underlying atherosclerosis. Few case reports of AMI in athletes taking anabolic androgenic steroids (AASs) have been reported so far. AAS-related AMI is possibly underreported in the medical literature due to the desire of the affected individuals to hide AAS use. Physicians should always consider the possibility of AAS abuse in the context of a young athlete suffering AMI. AASs can predispose to AMI through the acceleration of coronary atherosclerosis. Additionally, thrombosis without underlying atherosclerosis or vasospasm is highly possible to cause AMI in AAS users. Complications after AMI may be more frequent in AAS users.
The physiological QT prolongation in athletes is expected to widen the gray zone between physiology and pathology of QT, increasing the diagnostic challenges encountered in athletes with QT ...prolongation.
According to international recommendations for electrocardiogram in athletes, further evaluation for long QT syndrome (LQTS) is indicated in male athletes with corrected QT (QTc) ≥470 ms and in female athletes with QTc ≥480 ms. Apart from QTc ≥500 ms, diagnostic challenges arise in borderline cases of QTc prolongation, where further clinical investigations are needed to be performed to clarify whether LQTS exists. Clinical diagnostic investigations, including exercise testing, are more readily available, convenient, and easily interpretable, as well as less costly than genetic testing for LQTS. The main findings on exercise testing that are suggestive of LQTS can be the paradoxical prolongation of QTc during exercise and QTc ≥480 ms at fourth min of recovery.
Exercise testing appears to have an important role in the diagnostic evaluation of athletes with prolonged QT interval, when genetic testing is not available.
Growing analytical challenges have arisen for the detection of misuse of androgenic anabolic steroids (AAS) in athletes the last years. Therefore, consideration of additional indirect markers can ...substantially aid the efforts to detect AAS abuse in athletes. Moreover, this approach can also help physicians to suspect AAS abuse when treating athletes. Laboratory markers highly indicative of AAS abuse in athletes include the considerable downregulation of high density lipoprotein-cholesterol, elevation of haematocrit or serum γ-glutamyl transpeptidase levels and for males reduced serum levels of both luteinizing hormone and follicle-stimulating hormone. Moreover, physical signs suggestive of current AAS abuse are hypertension, apparent changes in behaviour making the athlete more irritable and aggressive and the sudden appearance of acne vulgaris in an adult athlete with no recent history of acne, while testicular atrophy and gynecomastia raise suspicion of current or past AAS abuse in male athletes.
This systematic review and meta-analysis aims to explore in heart failure (HF) patients with reduced ejection fraction (EF) undergoing exercise-based cardiac rehabilitation the following: 1) the ...comparison of temporal changes between peak oxygen uptake (VO2peak) and first ventilatory threshold (VO2VT1), 2) the association of VO2peak and VO2VT1 changes with physiological factors, and 3) the differential effects of continuous aerobic exercise (CAE) and interval training (IT) on VO2peak and VO2VT1.
A systematic literature search was conducted in PubMed, CENTRAL, and Scopus. Inclusion criteria were 1) original research articles using exercise-based cardiac rehabilitation, 2) stable HF patients with reduced EF, 3) available values of VO2peak and VO2VT1 (in mL/kg/min) both at baseline and after exercise training with comparison between these time points.
Among the 30 eligible trials, 24 used CAE, 5 IT, and one CAE and IT. Multivariable meta-regression with duration of exercise training and percentage of males as independent variables and the change in VO2peak as a dependent variable showed that the change in VO2peak was negatively associated with duration of exercise training (coefficient=-0.061, p=0.027), implying the possible existence of a waning effect of exercise training on VO2peak in the long term. Multivariable meta-regression demonstrated that both age (coefficient=-0.140, p<0.001) and EF (coefficient=-0.149, p<0.001) could predict the change in VO2VT1, whereas only age (coefficient=-0.095, p=0.022), but not EF (coefficient = 0.082, p = 0.100), could predict the change in VO2peak. The posttraining peak respiratory exchange ratio, as an index of maximum effort during exercise testing, correlated positively with the change in VO2peak (coefficient=-0.021, p=0.044). The exercise-induced changes of VO2peak (p = 0.438) and VO2VT1 (p = 0.474) did not differ between CAE and IT groups.
Improvement of endurance capacity during cardiac rehabilitation may be detected more accurately with the assessment of VO2VT1 rather than VO2peak.
The causes of the changes in peak oxygen uptake (VO2peak) and first ventilatory threshold (VO2VT1) during exercise-based cardiac rehabilitation in heart failure patients with reduced ejection fraction (EF). RER: respiratory exchange ratio. Display omitted
Can Noncardiac Syncope Occur during Exercise? Christou, Georgios A; Christou, Konstantinos A; Christou, Evangelos A ...
Cardiology,
01/2017, Letnik:
138, Številka:
3
Journal Article
Recenzirano
We describe the case of a 25-year-old athlete experiencing syncope during a 5-km running race. A thorough diagnostic workup reasonably excluded a cardiac disorder as the cause of syncope. The ...characterization of this episode of syncope as noncardiac appears to contradict the common belief that syncope during exercise has always a cardiac origin. Following a detailed history taking, it was revealed that the symptoms of the athlete started after a 180° turn of the route. This situation represents a setting relevant to a runner who stops suddenly after reaching the finish line and soon after experiences noncardiac syncope due to the abrupt cessation of muscle pump function of the lower limbs. Although the symptoms of the athlete in this report occurred during running, implying at a first glance the diagnosis of syncope occurring during exercise, a more detailed analysis of the circumstances indicated that these symptoms were in essence presenting after exercise from a pathophysiological view. The distinction between syncope occurring during and after exercise may be challenging enough for athletic activities involving a sudden stop of the running activity, such as for running races with sudden inversion of the route and sports characterized by rapid "starts and stops."
PDF
