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Biomedical subjects

D M Krikler

Publications and source records attributed to D M Krikler.

At least 19 recordsLinked to original sources
PubMed1993

Torsades de pointes.

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Diagnosis, Differential↗
PubMed1992

Atrial myxoma: a tumour in search of its origins.

OBJECTIVE: To determine whether atrial myxomas express antigens suggesting a neural origin. DESIGN: A retrospective analysis based on immunohistochemical examination of myxoma tissue. SETTING: Atrial myxomas excised by two tertiary referral cardiothoracic surgical units. SUBJECTS: 24 excised atrial myxomas. Three were from known cases of familial myxoma syndrome. METHODS: Immunohistochemical identifications of three neuroendocrine markers (protein gene product (PGP) 9.5, neurone specific enolase (NSE), synaptophysin) and S100 antigen; CD34 and von Willebrand factor; and chi smooth muscle actin to identify possible Schwann cell differentiation, endothelial cells, and smooth muscle cells respectively. RESULTS: The myxoma cells were PGP 9.5 positive in 18, S100 positive in 16, and NSE positive in 12. Of the 12 NSE positive myxomas seven were synaptophysin positive. All tumours that were NSE positive were also S100 and PGP 9.5 positive. The tumour surface was partially covered by myxoma cells, partly by endothelial cells. CONCLUSION: The histological appearances of myxomas with stellate cells embedded within a loose connective tissue stroma, abundant basophil cell infiltration, and the presence of pericellular type IV collagen are similar to nerve sheath tumours (neurofibromas) at other sites. A significant proportion of myxomas also express Schwann cell and neuroendocrine differentiation markers. These features cannot prove the origin of myxomas because tumours may develop aberrant phenotype expression but they do accord with the view that myxomas originate from endocardial sensory nerve tissue.

Antigens, Neoplasm↗
PubMed1990

The QRS complex.

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Bundle-Branch Block↗
PubMed1989

Comparative study of the effect of nifedipine versus diltiazem on exercise performance, serum propranolol levels, and ST-segment abnormalities in patients with chronic stable angina taking propranolol.

Twelve patients (10 men and 2 women), mean age 60.6 years (range 50 to 75), with stable angina pectoris were administered propranolol until beta blockade was evident. Treadmill exercise testing was performed, 24-hour ambulatory electrocardiograms were recorded, and serum propranolol levels were assessed at 1 and 2 hours after dosing with propranolol alone, and after 2 weeks of combined therapy with either nifedipine, 10 or 20 mg, or diltiazem, 60 or 120 mg, administered every 8 hours. Patients were assigned to treatment regimens in randomized, double-blind, crossover fashion. At the time of exercise testing, maximal exercise time, time to angina, peak exercise heart rate and systolic blood pressure and time to 1 mm of ST-segment depression were measured. The rate-pressure product was also calculated. Maximal exercise time increased from 708 +/- 140 seconds with propranolol alone to 795 +/- 156 seconds after combined propranolol-nifedipine therapy (p less than 0.05), and to 790 +/- 107 seconds (p less than 0.05) after propranolol-diltiazem therapy. Time to onset of angina increased from 472 +/- 191 seconds with propranolol alone to 564 +/- 123 seconds (p = NS) after propranolol-nifedipine treatment and to 607 +/- 197 seconds (p less than 0.05) after propranolol-diltiazem treatment. Peak exercise heart rate remained unchanged with propranolol-nifedipine therapy (103 +/- 16 beats/min vs 104 +/- 17 with propranolol alone). However, with propranolol-diltiazem therapy, peak exercise heart rate significantly decreased to 95 +/- 14 beats/min (p less than 0.05); peak systolic blood pressure and rate-pressure products were comparable on all treatment regimens.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

Community study of the causes of "natural" sudden death.

Three hundred and fifty cases of "natural" sudden death within six hours of onset of symptoms in people ranging in age from 18 to 69 years in Wandsworth were studied using a detailed necropsy protocol to determine the cause of death. Sudden death occurred in 28 (8%) Asians and blacks, but because of the small number they were excluded from the study, leaving 322 cases. Ischaemic heart disease accounted for 189 (59%) of the 322 sudden deaths (155 (65%) men; 34 (41%) women) and no proportional increase in instantaneous compared with non-instantaneous sudden death was found. Non-ischaemic cardiac disease was the cause of sudden death in 24 cases (7.5%). Non-cardiac disease included pulmonary emboli, aortic aneurysms, and intracerebral haemorrhage and caused 89 (27.6%) deaths. Alcohol was the cause of nine deaths (2.8%) and in 11 (3.4%) cases (six men and five women) no cause of death was found. This study shows that although ischaemic heart disease is the single largest cause of sudden natural death there are other major causes.

Adult↗
PubMed1988

The presence and molecular forms of cardiodilatin immunoreactivity in the human and rat right atrium.

A sensitive and specific radioimmunoassay has been developed for cardiodilatin, the N-terminal peptide sequence of the atrial natriuretic peptide (ANP) prohormone. Cardiodilatin-immunoreactivity (-IR) concentrations in the human right atrial appendage were found to correlate with ANP-IR concentrations, determined by an established radioimmunoassay, (cardiodilatin-IR = 13.2 +/- 1.2 nmol/g, ANP-IR = 19.8 +/- 2.0 nmol/g, r = 0.80, p less than 0.001). Characterisation of the cardiodilatin-IR in the human and rat right atrium by gel permeation and fast protein liquid chromatography revealed only two cardiodilatin-IR molecular forms. The larger more hydrophobic form, the majority of the cardiodilatin-IR, contained in addition ANP-IR and therefore represents the prohormone. The smaller, less hydrophobic form, lacked ANP-IR and thus represents the cleaved N-terminal peptide sequence of the prohormone. These findings indicate that the prohormone is the major molecular form in the human and rat atrium. Furthermore, they demonstrate that a single large N-terminal peptide, cardiodilatin, derived from the prohormone, may exist as a distinct molecular form in the atrium of these species.

Animals↗