Heart cardiac dysfunctions

The only way to determine if a comatose patient has SE is by EEG. EEG monitoring should be used for patients who remain unconscious after initial antiepileptic treatment, and for those who received a long-acting paralytic agent or require prolonged therapy for RSE. Treatment should never be delayed while awaiting EEG results. An electrocardiogram (ECG) should be obtained to rule out cardiac dysfunction when hypotension or an abnormal heart rate is observed. 

Ventricular assist devices can be used in the short-term (days to several weeks) for temporary stabilization of patients awaiting an intervention to correct the underlying cardiac dysfunction. They can also be used long term (several months to years) as a bridge to heart transplantation. Permanent device implantation has recently become an option for patients who are not candidates for heart transplantation. 

Y., Kawamura, N. Feldman, A. M., Tsutsui, H., Shimokawa, H., Takeshita, A., Involvement of inducible nitric oxide synthase in cardiac dysfunction with tumor necrosis factor-alpha, Am. J. Physiol. Heart Circ. Physiol. 282 (2002),... 

P MRS of the open-chested mouse at 4.7T. In a P MRSI study performed on a 9.4-T vertical-bore spectrometer, Flogel et al. were able to map localized energetics in several regions of the heart in a transgenic murine cardiomyopathy model. They found that cardiac dysfunction in the mutant was associated with impaired energy state. 

Toxicities included an infusion reaction consisting of fever, chills, pain, asthenia, nausea, and vomiting. This syndrome was typically observed after the initial infusion, was self-limited, and frequently did not recur with subsequent infusions. The most serious toxicity was cardiac dysfunction, defined as clinical findings of congestive heart failure and/or subclinical declines in cardiac ejection fraction, which was seen in 5% of patients. Cardiotoxicity was unanticipated, as it had not been detected in previous studies. The mechanism for this effect is unclear, but is likely related to trastuzumab s antiproferative effect on HER2-mediated homeostasis and response to injury. 

The mechanism responsible for PBN-induced cardiac dysfunction is unclear. In previous studies on free radical generation in the ischemic canine heart, hearts were perfused with 50 mmol/1 PBN and 50 mmol/1 MNP for 30 minutes prior to ischemia. It is possible that these high concentrations caused significant cardiac dysfunction and even injury to the heart prior to the ischemic insult. Similar concerns have also been expressed by Bolli et al. [110], In these studies the spin adduct subsequently detected in myocardial tissue by ESR spectroscopy during ischemia may have arisen, in part, as a consequence of the toxic effects of the spin traps. 

Rivers, J., Garrahy, R, Robinson, W., Murphy, A. Reversible cardiac dysfunction in hemochromatosis. Amer. Heart J. 1987 113 216-217... 

Ribbing s disease, which is characterized by multiple epiphyseal dystrophy. In a randomized, double-blind comparison of amlodipine (10 mg/day) and enalapril (20 mg/day) in 50 patients for 6 months, both drugs significantly reduced blood pressure, but amlodipine increased heart rate and plasma concentrations of noradrenaline and angiotensin II (7). These undesired effects make ACE inhibitors a better choice for prevention of cardiac dysfunction. 

Cardiac dysfunction, including congestive heart failure, particularly when combined with an anthracycline diarrhea... 

Shah AS, White DC, Emani S, et al. In vivo ventricular gene delivery of a p-adrenergic receptor kinase inhibitor to the failing heart reverses cardiac dysfunction. Circulation 2001 103 1311-1316. 

If the patient with coronary artery disease also develops cardiac dysfunction, the same medications would be expected to apply, but for additional reasons. The re-instation of preconditioning mechanisms by ACEI administration has already been described. (I-blockers have additional mechanisms, such as an antiapoptotic and antioxidant action.276 In this situation oxidative stress is also predominant and may further exacerbate apoptotic mechanisms.277 The only drugs predictably diminishing oxidative stress in clinical usage are carvedilol and statins. The latter drug family is also used in heart failure. Exercise is also a standard preventive and therapeutic intervention in both the above categories. 

A clinically relevant phenomenon is described in Chapter 5. Coronary microembolization which is a frequent event in ischemic heart disease due to plaque ruptures may compromise the microcirculation with subsequent events such as arrhythmias, cardiac dysfunction, infarcts and reduced coronary reserve. Furthermore, microembolization of coronary vasa vasorum may contribute to plaque instability and propagation of atherosclerosis into the more distal coronary vascular tree. Microembolization may offer an interpretation for some unexplained manifestations of ischemic heart disease in clinical practice. 

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