Cardiogenic shock after nifedipine administration in a pregnant patient: A case report and review of the literature

Botta, Ilaria; Devriendt, Jacques; Rodriguez, José Castro; Morissens, Marielle; Carling, Andrew; Gutierrez, Leonel Barreto; Préseau, Thierry; Bels, David De; Honoré, Patrick M.; Redant, Sébastien

doi:10.2478/jtim-2018-0029

Cited by 8 publications

(5 citation statements)

References 26 publications

(34 reference statements)

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“…It should be noted that reactions (6)-(8) are in consistence with known theoretical considerations (31) of Ca 2+ role in the regulation of CDB3 activity by corresponding kinases and phosphatases (52). Activation of the enzymes (kinases and phosphatases) by Ca 2+ is modeled in our work by Michaelis-Menten reaction (6), which formally describes stimulated activation of CDB3. We added reaction (8) of CDB3 spontaneous deactivation since our experimental data showed nonzero positive interception obtained by the theoretically linear dependence of the activation rate k on the inhibitor (nifedipine) concentration [I] (see Figs.…”

Section: Discussionmentioning

confidence: 59%

“…Other uses include painful spasms of the esophagus , Raynaud's phenomenon , tocolytic therapy . However, the effect of the treatment by nifedipine is not always positive . In particular, it is not clear the influence of nifedipine on the rate of HCO 3− / Cl − transmembrane CDB3 protein (AE1, Band 3), which plays an important role in bicarbonate metabolism .…”

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confidence: 99%

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Proposed Dynamics of CDB3 Activation in Human Erythrocytes by Nifedipine Studied with Scanning Flow Cytometry

et al. 2019

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Nifedipine is calcium channels and pumps blocker widely used in medicine. However, mechanisms of nifedipine action in blood are not clear. In particular, the influence of nifedipine on erythrocytes is far from completely understood. In this work, applying scanning flow cytometry, we observed experimentally for the first time the dynamics behind a significant increase of HCO 3 − /Cl − transmembrane exchange rate of CDB3 (main anion exchanger, AE1, Band 3, SLC4A1) of human erythrocytes in the presence of nifedipine in blood. It was found that the rate of CDB3 activation is not limited by the rate of nifedipine binding and/or Ca 2+ transport. In order to explain the experimental data, we suggested a kinetic model assuming that the rate of CDB3 activation is limited by the dynamics of the balance between two intracellular processes (1) the activation of CDB3 limited by its interaction with intracellular Ca 2+ , and (2) the spontaneous deactivation of CDB3. Thus the use of scanning flow cytometry allowed to clarify quantitatively the molecular kinetic mechanism of nifedipine action on human erythrocytes. In particular, the efficiency (~30) and rates of activation (~0.3 min −1 ) and deactivation (~10 −3 min −1 ) of CDB3 in human erythrocytes was evaluated for two donors.Nifedipine is widely used in medicine under the name of Adalat and other drugs. One common usage is the treatment of cardiovascular pathology such as atherosclerosis, coronary heart disease, hypertension, cerebral ischemia, and others (1). Other uses include painful spasms of the esophagus (2,3), Raynaud's phenomenon (4), tocolytic therapy (5). However, the effect of the treatment by nifedipine is not always positive (6). In particular, it is not clear (7) the influence of nifedipine on the rate of HCO 3− /Cl − transmembrane CDB3 protein (AE1, Band 3), which plays an important role in bicarbonate metabolism (8). Overall, a more complete understanding of nifedipine action in blood is needed.Nifedipine belongs to the subclass of dihydropyridines (DHPs), which are known as inhibitors of Ca 2+ transport across the erythrocyte membrane in both pathways: (1) inward leak through Ca 2+ entry channels (9-11), and (2) extrusion by plasma membrane Ca 2+ pumps (PMCA) (12,13). It was reported (13) that about 50% inhibition of PMCA was obtained at extracellular nifedipine concentration of 300 μM. Interestingly, the same extracellular concentration of 300 μM nifedipine was reported (14) to cause less (about 30%) inhibition of Ca 2+ entry channels of erythrocyte membrane. Stronger inhibition of PMCA than entry channels leads to the accumulation of intracellular Ca 2+ in erythrocytes in the presence of extracellular

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Section: Discussionmentioning

confidence: 59%

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confidence: 99%

Proposed Dynamics of CDB3 Activation in Human Erythrocytes by Nifedipine Studied with Scanning Flow Cytometry

et al. 2019

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“…In case of CCB overdose, intravenous calcium infusion is used (Salhanick & Shannon, ). Although cardiovascular toxicity by some CCBs is manifested by bradycardia and tachycardia, nifedipine, a vasodilator, does not have a direct effect on the heart but can induce reflex tachycardia (Botta et al, ). Guidelines of the Society of Critical Care Medicine recommends the use of catecholamines, such as norepinephrine or epinephrine, particularly norepinephrine to treat vasodilatory shock (Graudins et al, ).…”

Section: Discussionmentioning

confidence: 99%

Nifedipine toxicity is exacerbated by acetyl l‐carnitine but alleviated by low‐dose ketamine in zebrafish in vivo

Robinson

Tryndyak

et al. 2019

J of Applied Toxicology

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Calcium channel blocker (CCB) poisoning is a common and sometimes life-threatening emergency. Our previous studies have shown that acetyl L-carnitine (ALCAR) prevents cardiotoxicity and developmental toxicity induced by verapamil, a CCB used to treat patients with hypertension. Here, we tested whether toxicities of nifedipine, a dihydropyridine CCB used to treat hypertension, can also be mitigated by co-treatment with ALCAR. In the zebrafish embryos at three different developmental stages, nifedipine induced developmental toxicity with pericardial sac edema in a dose-dependent manner, which were surprisingly exacerbated with ALCAR co-treatment. Even with low-dose nifedipine (5 μM), when the pericardial sac looked normal, ALCAR cotreatment showed pericardial sac edema. We hypothesized that toxicity by nifedipine, a vasodilator, may be prevented by ketamine, a known vasoconstrictor. Nifedipine toxicity in the embryos was effectively prevented by co-treatment with low (subanesthetic) doses (25-100 μM added to the water) of ketamine, although a high dose of ketamine (2 mM added to the water) partially prevented the toxicity.As expected of a CCB, nifedipine either in the presence or absence of ketamine-reduced metabolic reactive oxygen species (ROS), a downstream product of calcium signaling, in the rapidly developing digestive system. However, nifedipine induced ROS in the trunk region that showed significantly stunted growth indicating that the tissues under stress potentially produced pathologic ROS. To the best of our knowledge, these studies for the first time show that nifedipine and the dietary supplement ALCAR together induce adverse effects while providing evidence on the therapeutic efficacy of subanesthetic doses of ketamine against nifedipine toxicity in vivo.

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“…This can predict whether there is no reflow or slow blood flow after stent implantation. At present, the prevention and treatment of microcirculatory disorders and coronary no reflow are limited[26-32]. Therefore, in patients with hyperthrombotic lesions that achieve complete recanalization of infarcted coronary arteries, pre-coronary administration of drugs, such as glycoprotein IIb/IIIa receptor antagonists or sodium nitroprusside, should be fully evaluated based on the nature of the thrombus extracted from the coronary arteries.…”

Section: Discussionmentioning

confidence: 99%

Correlation between intracoronary thrombus components and coronary blood flow after percutaneous coronary intervention for acute myocardial infarction at different onset time

Zhang

Liu

et al. 2019

WJCC

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BACKGROUND Acute myocardial infarction (AMI) is a leading cause of mortality. Early reperfusion to restore blood flow is crucial to successful treatment. In the current reperfusion regimen, an increasing number of patients have benefited from direct percutaneous coronary intervention (PCI). In order to understand whether there is a correlation between the components of coronary thrombosis and the absence of reflow or slow blood flow after coronary stent implantation in direct PCI, we collected data on direct PCI cases in our hospital between January 2016 and November 2018. AIM To investigate the correlation between intracoronary thrombus components and coronary blood flow after stent implantation in direct PCI in AMI. METHODS We enrolled 154 patients (85 male and 69 female, aged 36–81 years) with direct PCI who underwent thrombus catheter aspiration within < 3, 3–6 or 6–12 h of onset of AMI between January 2016 and November 2018. The thrombus was removed for pathological examination under a microscope. The patients of the three groups according to the onset time of AMI were further divided into those with a white or red thrombus. The thrombolysis in myocardial infarction (TIMI) blood flow after stent implantation was recorded based on digital subtraction angiography during PCI. The number of patients with no-reflow and slow blood flow in each group was counted. Statistical analysis was performed based on data such as onset time, TIMI blood flow. RESULTS There were significant differences in thrombus components between the patients with acute ST-segment elevation myocardial infarction and non-ST-segment elevation myocardial infarction ( P < 0.01). In the group with PCI < 3 h after onset of AMI, there was no significant difference in the incidence of no-reflow and slow-flow between the white and red thrombus groups. In the groups with PCI 3-6 and 6-12 h after onset of AMI, there was a significant difference in the incidence of no-reflow and slow-flow between the white and red thrombus groups ( P < 0.01). There was a significant correlation between the onset time of AMI and the occurrences of no-reflow and slow blood flow during PCI ( P < 0.01). CONCLUSION In direct PCI, the onset time of AMI and color of coronary thrombus are often used to predict whether there will be no reflow or slow blood flow after stent implantation.

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Cardiogenic shock after nifedipine administration in a pregnant patient: A case report and review of the literature

Cited by 8 publications

References 26 publications

Proposed Dynamics of CDB3 Activation in Human Erythrocytes by Nifedipine Studied with Scanning Flow Cytometry

Proposed Dynamics of CDB3 Activation in Human Erythrocytes by Nifedipine Studied with Scanning Flow Cytometry

Nifedipine toxicity is exacerbated by acetyl l‐carnitine but alleviated by low‐dose ketamine in zebrafish in vivo

Correlation between intracoronary thrombus components and coronary blood flow after percutaneous coronary intervention for acute myocardial infarction at different onset time

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