Electrocardiographic changes during sustained normobaric hypoxia in patients after myocardial infarction
Tilmann KramerJan‐Niklas HönemannHenning WeisFabian HoffmannStephan RosenkranzStephan BaldusMartin HellmichBenjamin D. LevineJens JordanJens TankUlrich Limper
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Abstract:
The safety of prolonged high-altitude stays and exercise for physically fit post-myocardial infarction (MI) patients is unclear. Myocardial tissue hypoxia and pulmonary hypertension can affect cardiac function and electrophysiology, possibly contributing to arrhythmias. We included four non-professional male athletes, clinically stable after left ventricular MI (three with ST-segment elevation MI and one with non-ST-segment elevation MI) treated with drug-eluting stents for single-vessel coronary artery disease. Oxygen levels were reduced to a minimum of 11.8%, then restored to 20.9%. We conducted electrocardiography (ECG), ergometry, and echocardiography assessments in normoxic and hypoxic conditions. With an average age of 57.8 ± 3.3 years and MI history 37 to 104 months prior, participants experienced a significant increase in QTc intervals during hypoxia using Bazett's (from 402 ± 13 to 417 ± 25 ms), Fridericia's (from 409 ± 12 to 419 ± 19 ms), and Holzmann's formulas (from 103 ± 4 to 107 ± 6%) compared to normoxia. This effect partially reversed during recovery. Echocardiographic signs of pulmonary hypertension during normobaric hypoxia correlated significantly with altered QTc intervals (p < 0.001). Despite good health and complete revascularization following MI, susceptibility to hypoxia-induced QTc prolongation and ventricular ectopic beats persists, especially during physical activity. MI survivors planning high-altitude activities should consult cardiovascular specialists with high-altitude medicine expertise.Keywords:
Hypoxia
Short QT syndrome
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Abstract We report the change in the QT interval in 84 adult patients with SARS-CoV-2 infection treated with Hydroxychloroquine/Azithromycin combination. QTc prolonged maximally from baseline between days 3 and 4. in 30% of patients QTc increased by greater than 40ms. In 11% of patients QTc increased to >500 ms, representing high risk group for arrhythmia. The development of acute renal failure but not baseline QTc was a strong predictor of extreme QTc prolongation.
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Hypoxia
Fetal growth
Fetal hypoxia
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Establishment of a new formula for QT interval correction using a large colony of cynomolgus monkeys
The demand for monkeys for medical research is increasing, because their ionic mechanism of repolarization is similar to that of humans. The QT interval is the distance between the Q wave and T wave, but this interval is affected by heart rate. Therefore, QT correction methods are commonly used in clinical settings. However, an accurate correction formula for the QT interval in cynomolgus monkeys has not been reported. We assessed snapshot electrocardiograms (ECGs) of 353 ketamine-immobilized monkeys, including aged animals, and contrived a new formula for the corrected QT interval (QTc) as a marker of QT interval prolongation in cynomolgus monkeys. Values for QTc were calculated using the formula [QTc] = [QT] / [RR]n, along with several other formulas commonly used to calculate QTc. We found that the optimal exponent of the QT interval corrected for heart rate, n, was 0.576. The mean value of QTc in healthy monkeys determined using the new formula was 373 ± 31 mm, and there were no significant differences between the sexes. Other ECG parameters were not significantly different between the sexes and there were no age-related effects on QTc. Prolongation of QTc to over 405 ms, as calculated by the new formula, was observed in 50 monkeys with underlying diseases. Additionally, all monkeys with QTc above 440 ms by the new formula had some underlying disease. The results resemble those in humans, suggesting that the new QTc formula could be useful for diagnosis of QT interval prolongation in cynomolgus monkeys.
Prolongation
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The episode of prolonged exposure to high altitude can cause hypoxia and potential significant health consequences. In people with high altitude disorder, the body reaction to high altitudes starts with the formation of a protein called hypoxia-inducible factor (HIF), which triggers a series of other physiological changes and plays a central role in the hypoxia response; its activity is regulated by the oxygen-dependent degradation of the HIF-1α protein. This deserving condition provides an opportunity to study the effect of low oxygen tension of flying at high altitude that could lead to hypoxia using hypoxia sensor.
Hypoxia
Oxygen tension
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急性前壁梗塞において, 前胸壁QT時間の空間的分布 (前胸壁QT interval map) とその経時的変動, および前胸壁QT interval map所見と急性期心室性不整脈重症度との関連を検討した.正常20例と急性前壁梗塞32例で, 入院時, 発症後24時間, 72時間に前胸壁36点から心電図を記録, 各点のQTcから前胸壁QT interval mapを作成した.また発症後1週間の心室性不整脈の重症度により3群に分類した.結果 (1) 急性前壁梗塞では入院時 (発症後平均5時間) にV2～V4領域で最短QTを, 24時間後には同部で最長QTを示す例が多く, 最長, 平均および最長と最短の差のQTは入院時に正常者より大で, 24時間後に著明に延長し, 72時間後には短縮した. (2) 入院時の前胸壁QT interval map上, 最長および差のQTは心室頻拍群で有意に延長し, 最長QT0.48秒以上かつ差のQT0.08秒以上を示す例が多かった.急性前壁梗塞の前胸壁QT時間は正常例と異なり, 特徴的な空間的分布と経時的変動を示し, 発症早期の前胸壁QT interval mapは急性期心室性不整脈重症度判定に有用と考えられた.
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High-altitude hypoxia causes intrauterine growth restriction and cardiovascular programming. However, adult humans and animals that have evolved at altitude show certain protection against the effects of chronic hypoxia. Whether the highland fetus shows similar protection against high altitude gestation is unclear. We tested the hypothesis that high-altitude fetal sheep have evolved cardiovascular compensatory mechanisms to withstand chronic hypoxia that are different from lowland sheep. We studied seven high-altitude (HA; 3600 m) and eight low-altitude (LA; 520 m) pregnant sheep at ∼90% gestation. Pregnant ewes and fetuses were instrumented for cardiovascular investigation. A three-period experimental protocol was performed in vivo: 30 min of basal, 1 h of acute superimposed hypoxia (∼10% O2) and 30 min of recovery. Further, we determined ex vivo fetal cerebral and femoral arterial function. HA pregnancy led to chronic fetal hypoxia, growth restriction and altered cardiovascular function. During acute superimposed hypoxia, LA fetuses redistributed blood flow favouring the brain, heart and adrenals, whereas HA fetuses showed a blunted cardiovascular response. Importantly, HA fetuses have a marked reduction in umbilical blood flow versus LA. Isolated cerebral arteries from HA fetuses showed a higher contractile capacity but a diminished response to catecholamines. In contrast, femoral arteries from HA fetuses showed decreased contractile capacity and increased adrenergic contractility. The blunting of the cardiovascular responses to hypoxia in fetuses raised in the Alto Andino may indicate a change in control strategy triggered by chronic hypoxia, switching towards compensatory mechanisms that are more cost-effective in terms of oxygen uptake.
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Intrauterine growth restriction
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Climbing to a high altitude causes breathing to shorten, which reduces the amount of oxygen in the tissues and causes hypoxia. High altitude sickness is a medical illness with lethal implications such as hypoxia, high altitude pulmonary oedema (HAPE), high altitude cerebral oedema (HACE), and several other neurological disorders. Acclimatization is a primary response that encounters hypoxia and during this time individuals adapt to the decreased level of oxygen at a specific height. To investigate this physiological process, several studies have been conducted in the last few years. These studies have indicated the changes in the transcriptional and translational levels of various stress-associated genes/proteins under hypoxia and hypoxia acclimatization. Reducing air pressure at high altitudes causes hypoxia, which is a potential threat to the normal functioning of the brain. The generation of excessive free radicals and their intracellular diffusion leads to oxidative stress. Recent studies on molecular signalling along with shreds of evidence from cognitive impairment in the animal model during hypoxia have demonstrated that the cortex and hippocampus as anatomically and biochemically most vulnerable to oxidative stress in contrast to other regions of the brain. The emerging tools such as omics can be a milestone to study the physiological response of high altitudes and can decrease the adaptation time at high altitudes.
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