Myocardial infarction (MI) is a leading cause of heart failure and death worldwide. Preservation of contractile function and protection against adverse changes in ventricular architecture (cardiac remodeling) are key factors to limiting progression of this condition to heart failure. Consequently, new therapeutic targets are urgently required to achieve this aim. Expression of the Runx1 transcription factor is increased in adult cardiomyocytes after MI; however, the functional role of Runx1 in the heart is unknown.
High-intensity interval training (HIIT) with interspersing active recovery is an effective mode of exercise training in cohorts ranging from athletes to patients. Here, we assessed the intensity-dependence of the intervals and active recovery bouts for permitting a sustainable HIIT protocol.Fourteen males completed 4x4-minute HIIT protocols where intensities of intervals ranged 80-100% of maximal oxygen uptake (VO2max) and active recovery ranged 60-100% of lactate (La-) threshold (LT). Blood La- measurements indicated fatigue, while tolerable duration of intervals indicated sustainability.HIIT at 100% of VO2max allowed 44±10% [30-70%] completion, i.e. fatigue occurred after 7minutes:6seconds of the intended 16 minutes of high intensity, whereas HIIT at 95-80% of VO2max was 100% sustainable (P<0.01). Measured intensity did not differ from intended intensity across the protocols (P>0.05). Blood La- concentration [La-] increased to 9.3±1.4mM during HIIT at 100% of VO2max, whereas at 80-95% of VO2max stabilized at 2-6mM in an intensity-dependent manner (P<0.01 vs. 100% of VO2max and P<0.05 vs. baseline). Active recovery at 60-70% of LT during HIIT associated with steady-state blood [La-] peaking at 6-7mM, whereas at 80-100% of LT, blood [La-] accumulated to 10-13mM (P<0.05). After HIIT, active recovery at 80-90% of LT cleared blood [La-] 90% faster than at 60-70% of LT (P<0.05).To permit highest exercise stress during 4x4-minute HIIT, exercise intensity should be set to 95% of VO2max, whereas active recovery should be set to 60-70% of LT during HIIT and 80-90% of LT after HIIT to most efficiently prevent excess La- and aid recovery.
Heart Failure (HF) and Atrial Fibrillation (AF) are concomitant in many patients. They share common risk factors and can exacerbate or precipitate each other. The aim of this study was to examine the management of patients presenting to Letterkenny University Hospital who were assessed to have tachycardia-induced cardiomyopathy.
Methods
Patients known to the heart failure support service that had a diagnosis of tachycardia-induced cardiomyopathy were included in this review. Additionally, a HIPE search was undertaken for primary admissions for AF and secondary diagnosis of HF and the medical clinical file reviewed. Patients with known ischaemic heart disease or preserved ejection fraction HF were excluded. Data was analysed using SPSS.
Results
48 patients were identified, with a mean age of 67 yrs. The majority had AF and HF diagnosed on the same admission. Hypertension was the most common comorbidity. 96% of patients had an ejection fraction (EF) of <40% at presentation. The majority of patients were appropriately anti-coagulated and had appropriate levels of HF medications (ACE-I/Beta-blockers/MRA). 44% underwent direct current cardioversion with an additional 6% reverting to sinus rhythm chemically or spontaneously. While the total group showed increased EF at one year, those who remained in SR had markedly better improvements with only 12% remaining at EF < 40% compared to 46% of those who were in AF at follow up.
Conclusion
Tachycardia induced cardiomyopathy is a potentially reversible cause of heart failure and when sinus rhythm is restored it resulted in substantial increases in EF. This group of patients should be identified for early rhythm control in order to improve outcomes.
Accidental hypothermia is associated with increased risk for arrhythmias. QRS/QTc is proposed as an ECG-marker, where decreasing values predict hypothermia-induced ventricular arrhythmias. If reliable it should also predict nonappearance of arrhythmias, observed in species like rat that regularly tolerate prolonged hypothermia. A rat model designed for studying cardiovascular function during cooling, hypothermia and subsequent rewarming was chosen due to species-dependent resistance to ventricular arrhythmias. ECG was recorded throughout the protocol. No ventricular arrhythmias occurred during experiments. QRS/QTc increased throughout the cooling period and remained above normothermic baseline until rewarmed. Different from the high incidence of hypothermia-induced ventricular arrhythmias in accidental hypothermia patients, where QRS/QTc ratio is decreased in moderate hypothermia; hypothermia and rewarming of rats is not associated with increased risk for ventricular fibrillation. This resistance to lethal hypothermia-induced arrhythmias was predicted by QRS/QTc.
Background: Ventricular arrhythmias and cardiac arrest emerge as the most important complication when rewarming victims of accidental hypothermia. Pharmacological treatment and prevention of such arrhythmias remains challenging and the underlying mechanisms are unclear. This randomized, experimental study assessed cardiac electrophysiology to find potential pharmacological strategies at temperatures occurring in therapeutic and accidental hypothermia.
Hypothermia is defined as a core body temperature of 35°C or less and can be
induced (i.e. therapeutic) or accidental. It is well established that hypothermia
leads to a positive inotropic response which causes an increase in the magnitude
of cardiac contraction, however rewarming from hypothermia is associated with
a negative inotropic response, and the underlying mechanisms of this remain
unclear. Accidental hypothermia is further complicated by risk of ventricular
arrhythmias and cardiac arrest. This contributes to high mortality rates among
these patients. Although hypothermia is used extensively as a therapeutic
intervention and survival is possible after extreme exposure, treatment of
arrhythmias during rewarming is still challenging. In order to develop targeted
anti-arrhythmic strategies in this very specific situation, we first need to
understand the basis for pro-arrhythmia during cooling and rewarming. This
study aimed to examine the effect of hypothermia and rewarming on aspects of
cardiac inotropy and excitability.
An in vitro model of hypothermia and rewarming using isolated rat ventricular
cardiomyocytes showed that following 3 hours of hypothermia there was a
significant reduction in shortening upon rewarming. This was not accompanied
by a change in intracellular Ca2+, suggesting a rewarming induced decrease in
myofilament sensitivity to Ca2+. In separate experiments, animals underwent an
in vivo hypothermia/rewarming procedure and displayed evidence of rewarming
induced contractile dysfunction. Epicardial action potential (AP) measurements
on these hearts showed a shortened AP duration (APD) when compared to
normothermic control animals, which suggests that a sustained
electrophysiological effect that could manifest as a shortened QT interval. In
contrast to this, a period of transient hypothermia had alternative detrimental
effects on the cardiac APD when compared to prolonged hypothermia, an effect
that could predispose to the induction of long QT related arrhythmias and
ventricular tachycardia.
Separate experiments assessed the effect of moderate (31˚C) and severe (17˚C)
hypothermia on cardiac excitability in Langendorff perfused rabbit hearts.
Moderate hypothermia prolonged PR and QT intervals whilst in severe
hypothermia all ECG parameters were prolonged. Ventricular activation times
were unaffected at 31°C whilst action potential duration (APD90) was
significantly prolonged. At 17°C there were significant and proportionally similar
delays in both activation and repolarisation. Ventricular fibrillation (VF)
threshold was significantly reduced at 31°C (pro-arrhythmic), but at 17°C VF
threshold was >2x baseline (37°C) (anti-arrhythmic). At 31°C, transverse
conduction (CVt) was relatively insensitive to cooling versus longitudinal
conduction (CVl) but at 17°C both CVt and CVl were proportionately reduced to a
similar extent. The gap junction uncoupler heptanol had a larger relative effect
on CVt than CVl, and at 31°C was able to restore the CVt/CVl ratio, returning VF
threshold to baseline values. This suggests that moderate hypothermia creates
repolarisation abnormalities and is pro-arrhythmic. These divergent effects
appear to be linked to a lower temperature sensitivity of gap junctions, a
conclusion supported by the anti-arrhythmic effect of heptanol at 31°C.
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