The Prognosis for Patients Referred with Suspected Acute Myocardial Infarction

ABSTRACT. Engby B, Strunge P, Olsen J. (Department of Internal Medicine, Horsens Hospital, Horsens, Denmark.) The prognosis for patients referred with suspected acute myocardial infarction. A follow-up investigation of the prognosis of 381 patients admitted with suspected acute myocardial infarction (AMI) has been carried out in respect of later AMI or death. During hospitalization the patients were divided into groups with particular attention to patients with no demonstrable myocardial infarction but with ischaemic heart disease (non-AMI) and patients with confirmed AMI. All patients were subjected to follow-up for 43 months (range 37–54). The mortality from cardiovascular causes after four years was 26.2% of 130 non-AMI patients and 25.8% of AMI patients. The majority of new infarctions were found in the AMI patients, but with even increase in both groups, 50% occurring within the first 12 months. The groups were studied with regard to earlier manifestations of ischaemic heart disease and heart failure during hospitalization, without any difference being observed. Due to the poor prognosis the question is raised whether non-AMI patients as a group should be offered prophylactic therapy.     

Autonomic Dysfunction and New‐Onset Atrial Fibrillation in Patients With Left Ventricular Systolic Dysfunction After Acute Myocardial Infarction: A CARISMA Substudy

Predicting New‐Onset AF. Background: Atrial fibrillation (AF) increases morbidity and mortality in patients with previous myocardial infarction and left ventricular systolic dysfunction. The purpose of this study was to identify patients with a high risk for new‐onset AF in this population using invasive and noninvasive electrophysiological tests. Methods: The study included 271 patients from the Cardiac Arrhythmias and RIsk Stratification after Myocardial InfArction (CARISMA) study with an acute myocardial infarction (AMI) and left ventricular ejection fraction ≤40% without previous AF at enrollment. Within 21 days after the AMI, an implantable loop recorder was inserted and used to diagnose AF over the 2‐year study duration. The following tests were performed: heart rate variability (HRV) and turbulence (HRT) analyses from repeated 24‐hour Holter recordings, 2‐dimensional (2D)‐echocardiograms, exercise test, and programmed electrophysiologic stimulation. Results: A total of 101 patients (37%) developed AF during the study. Predictive measures included several indexes of HRV including reduced low‐frequency (LF) power from spectral HRV analysis (adjusted HR = 1.6, P = 0.034), HRT slope ≤2.5 (HR = 1.6, P = 0.032) and Detrended Fluctuation Analysis (DFA1) from HRV analysis (HR = 1.8, P = 0.011); all are measures of cardiac autonomic nervous system dysfunction. Combined with age >60 years, low values for LF, HRT slope, and DFA1 provided a powerful risk score for prediction of new‐onset AF (1–2 points: HR = 4.3, P = 0.001, 3–4 points: HR = 7.0, P < 0.001). Conclusion: Abnormal HRV and HRT parameters, which are associated with disturbances in the cardiac autonomic regulation, are associated with increased risk of new‐onset AF independently of conventional clinical risk variables. (J Cardiovasc Electrophysiol, Vol. 21, pp. 983‐990, September 2010)     

Unilateral overgrowth and remodeling processes after fracture of the mandibular condyle

abstract – An overgrowth of the fractured side of the mandible coincided with the general skeletal growth spurt during puberty in two boys with unilateral fracture of the condylar neck and dislocation of the condyle. In one of the cases is demonstrated the formation of a condyle-like bony process and resorption of the dislocated condyle, which took place within a few months after fracture. The observation of mandibular overgrowth indicates that if no functional disorders necessitate interference, facial asymmetry after fracture of the condylar neck should not be corrected surgically in young persons until the prognosis of mandibular growth is estimated by means of cephalometric radiographic analysis.     

METABOLIC ALKALOSIS IN INFANTS: ROLE OF WATER DEPLETION AND CHANGES IN COMPOSITION OF STOOL

Simple calculations of the effect of volume depletion on the concentration of titratable base of blood show this effect to be largely adequate to account for commonly observed degrees of metabolic alkalosis in patients with mild or extreme dehydration due to obstructive vomiting. This suggests that hydrochloric acid depletion per se may not be a major determinant of the blood acid-base status in such conditions. Clearly, part of the base equivalents missing in the extracellular fluid may be sought in the cell water; but currently available evidence concerning gastrointestinal transport of acid and base invites a conception of gastrointestinal acid-base homeostasis–and the hypothesis that in obstructive vomiting changes in the composition of stool may appreciably modify the effect of gastric hydrochloric acid depletion. In studies of intracellular buffering and net base balance in gastric alkalosis, it must be realized that the primary extracellular disturbance may be largely contractional and that stool losses (or luminal pooling) of base may be an important variable.     

Visual Disturbances and Occipital Brain Infarct Following Acute,Transient Hypotension in Hypertensive Patients

ABSTRACT In four hypertensive patients, acute lowering of blood pressure by therapeutic or diagnostic procedures caused visual disturbances ranging from transient visual hallucinations to severe, long-lasting visual impairment. These symptoms were associated with occipital lobe cerebral infarcts that tended to occur in the border zones between the major cerebral arteries. The infarcts may be seen as the combined result of a “watershed” effect during acute hypotension and the presence of structural hypertensive vascular adaptation. When a hypertensive patient complains of visual disturbances during acute blood pressure lowering, the pressure should be allowed to settle at a level somewhat above normal.     

The Familial Magnesium-losing Kidney

ABSTRACT. Magnesium deficiency is often secondary to existing disease. Over a period of 20 years, 17 cases of primary magnesium-losing kidney have been reported. This report describes two additional cases, and a comparison with previous cases is made. The familial magnesiumlosing kidney appears to be caused by a congenital tubular defect in the reabsorption of magnesium. Its manifestations may be various but the diagnosis is established by the presence of Hypomagnesemia with an unappropriately high urinary magnesium excretion in patients with no other renal disorder.