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Hannu Parikka

Publications and source records attributed to Hannu Parikka.

5 recordsLinked to original sources
PubMed2005

Transcardiac gradients of N-terminal B-type natriuretic peptide in aortic valve stenosis.

BACKGROUND: Plasma B-type natriuretic peptide (BNP), as well as the N-terminal part of the prohormone (Nt-BNP), are frequently elevated in aortic valve stenosis (AS). Yet, their release from the heart into the circulation has never been directly studied in AS. AIM: To assess the release of Nt-BNP in AS with focus on the identification of its main determinants. METHODS: We studied 49 adult patients undergoing preoperative cardiac catheterization for isolated AS. Blood was sampled from the aortic root and the coronary sinus for Nt-BNP determination by immunoassay. RESULTS: The mean (+/-S.E.) transcardiac Nt-BNP step-up averaged 79+/-53 pmol/l in 11 control patients free of structural heart disease, 75+/-32 pmol/l in 31 AS patients free of heart failure (HF), 236+/-62 pmol/l in 8 AS patients with diastolic HF (ejection fraction > or = 50%, pulmonary wedge pressure > 14 mm Hg) and 469+/-66 pmol/l in 7 AS patients with systolic HF (ejection fraction < 50%, wedge pressure > 14 mm Hg) (p<0.001). The transcardiac Nt-BNP gradient was independently associated with left ventricular (LV) end-diastolic pressure (beta=0.47, p<0.001) and ejection fraction (beta=-0.29, p<0.019) and with co-existent coronary artery disease (beta=0.23, p=0.050). CONCLUSION: LV diastolic and systolic dysfunction along with coronary artery disease are likely to be the key determinants of cardiac Nt-BNP release in AS. The transcardiac Nt-BNP gradient increases on average three-fold with the development of diastolic HF and six-fold in systolic HF.

Aged↗
PubMed2004

Atrial refractoriness and action potential duration after sudden reversal of atrioventricular sequence.

To address the potential of atrioventricular (AV) asynchrony to provoke cardiac arrhythmias, atrial electrophysiology was examined during normal and reversed AV interval in anesthetized pigs. A new automatic stimulation technique was adapted to monitor rapid changes in the effective refractory period (ERP), using continuous AV sequential pacing, incremental extrastimulus interval scanning, and automatic detection of capture. Right atrial ERP using 2-8 ms stimulus interval increments and right atrial and ventricular monophasic action potential (MAP) duration were determined simultaneously when the AV interval was changed from normal (+80 ms) to reversed (-40 ms) and back. During reversed AV interval the peak right atrial pressure increased from 8 +/- 3 to 14 +/- 4 mmHg (P < 0.001) and mean arterial pressure decreased from 86 +/- 18 to 65 +/- 21 mmHg (P < 0.001). At new steady state, atrial ERP and MAP duration at 90% level of repolarization were lengthened by 22 +/- 16 and 42 +/- 12 ms respectively (P < 0.001). Ventricular MAP duration did not change. A statistically significant lengthening in atrial ERP could be demonstrated in 5-10 seconds. After reversion of the AV sequence, the ratio of atrial ERP to MAP duration decreased from 1.27 to 0.94 (P < 0.001) on average for 15 seconds, the change being thought to favor reentry. Thus atrial wall stress from contraction during ventricular systole even for a short period of time modifies atrial electrophysiology. Deficient AV synchrony may immediately contribute to the development of atrial arrhythmias.

Action Potentials↗
PubMed2003

[Fainting].

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Diagnosis, Differential↗
PubMed2002

Detection of rapid changes in ventricular refractoriness in human studies.

Conventional determination of the ventricular effective refractory period (VERP) is unsuitable for detection of rapid fluctuations in the effective refractory period (ERP). A programmed stimulation system was developed that adapts continuous atrioventricular sequential pacing, incremental extrastimulus interval (S1S2) scanning, and automatic detection of extrastimulus capture which is followed by shortening of S1S2 to execute repeated scanning. The accuracy of ERP determination was tested using variable incremental (2 and 4 ms) and decremental (4-16 ms) steps of the S1S2 interval. Based on a mean of 82 determinations in eight patients, the average VERP values stayed at 249.8-251.0 ms except during the highest capture frequency. Standard deviation of ERP values ranged from 1.1 to 2.5 ms on average at the tested incremental and decremental steps. One determination was accomplished within 7.8-15.6 seconds on average. The ability to track changes in ERP was tested by changing the drive cycle length. Time constants for the adaptation rate of VERP and ventricular monophasic action potential duration at a 90% level of repolarization were determined from each test, and were similar, 51 +/- 8 seconds (mean +/- SEM) for ERP and 51 +/- 6 seconds for the action potential duration. Thus, the developed method provides accurate ERP measurements during rapid variation in ventricular refractoriness. It allows studying the recovery of excitability and the action potential duration simultaneously, and would be valuable particularly in pathological conditions and pharmacologic interventions where these electrophysiological variables become dissociated.

Action Potentials↗