title: Acute effects of smoking on diastolic function in healthy participants: studies by conventional doppler echocardiography and doppler tissue imaging.
abstract: The acute effects of smoking on left ventricular (LV) function were studied in 36 healthy participants (mean age 38 +/- 10 years). The studies were made before and immediately and 30 minutes after smoking a cigarette. From apical 4- and 2-chamber views, the mitral annular velocities, determined by pulsed wave Doppler tissue imaging, were measured at 4 LV sites corresponding to the septum and the anterior, lateral, and inferior walls. A mean value from the 4 sites was used to assess LV function. The peak systolic, early diastolic, late diastolic, and the ratio of early to late diastolic velocities were recorded. In addition, other conventional Doppler echocardiographic diastolic parameters were also determined. Heart rate was increased immediately after smoking (from 67 +/- 8 to 74 +/- 10 bpm, P <.001). There was no change in systolic mitral annular velocity. Diastolic LV function was changed significantly immediately after smoking. The transmitral A wave increased (0.55 +/- 0.1 vs 0.7 +/- 0.1 m/s, P <.001), the transmitral E/A ratio decreased (1.5 +/- 0.6 vs 1.1 +/- 0.3, P <.001), and the transmitral E-wave deceleration time increased (186 +/- 42 vs 211 +/- 44 ms, P <.05). The diastolic myocardial velocity at the mitral annulus also changed significantly: the early diastolic velocity decreased (16 +/- 3 vs 15 +/- 3 cm/s, P <.001), the late diastolic velocity increased (10.9 +/- 2.2 vs 12 +/- 2.4 cm/s, P <.001), and the ratio of early to late diastolic annular velocities decreased (1.5 +/- 0.5 vs 1.2 +/- 0.4, P <.001). The changes in the transmitral flow velocities remained unaltered even 30 minutes afterward, although the heart rate returned to normal. The results were similar in both smokers and nonsmokers. Acute smoking of a cigarette influences LV diastolic function in healthy participants. The mechanism behind this effect cannot be explained only by changes in the heart rate or loading conditions. The mechanism is probably more complex.
authors.affiliation: Department of Cardiology, Karolinska Institute at South Hospital (Södersjukhuset), Stockholm. mahbubul.alam@medklin.sos.sll.se
authors.forename: Mahbubul
authors.initials: M
authors.lastname: Alam
authors.forename: Bassem A
authors.initials: BA
authors.lastname: Samad
authors.forename: Johan
authors.initials: J
authors.lastname: Wardell
authors.forename: Eva
authors.initials: E
authors.lastname: Andersson
authors.forename: Christer
authors.initials: C
authors.lastname: Höglund
authors.forename: Rolf
authors.initials: R
authors.lastname: Nordlander
mesh_terms: D000328:Adult; D000367:Age Factors; D001783:Blood Flow Velocity / Q000187:drug effects / Q000502:physiology; D003971:Diastole / Q000187:drug effects / Q000502:physiology; D015150:Echocardiography, Doppler; D005260:Female; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006801:Humans; D007089:Image Enhancement; D008297:Male; D008875:Middle Aged; D008943:Mitral Valve / Q000000981:diagnostic imaging / Q000503:physiopathology; D015588:Observer Variation; D012016:Reference Values; D012907:Smoking / Q000009:adverse effects* / Q000503:physiopathology; D013599:Systole / Q000187:drug effects / Q000502:physiology; D018084:Ultrasonography, Interventional; D016277:Ventricular Function, Left / Q000187:drug effects* / Q000502:physiology*